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Achilles tendinopathy: new insights in cause of pain, diagnosis and management

van Sterkenburg, M.N.

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Citation for published version (APA):van Sterkenburg, M. N. (2012). Achilles tendinopathy: new insights in cause of pain, diagnosis andmanagement.

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Achilles tendinopathyNew insights in cause of pain,

diagnosis and management

M.N. van Sterkenburg

Achilles tendinopathy: new insights in cause of pain, diagnosis and management

Maayke van Sterkenburg

PhD thesis, University of Amsterdam, the Netherlands

©2012, M.N. van Sterkenburg, Amsterdam, the Netherlands

This thesis was prepared at the Orthopaedic Research Center Amsterdam, Academical Medi-

cal Center, University of Amsterdam, the Netherlands

This thesis was supported by Stichting Steun Orthopaedie AMC

The publication of this thesis was supported by Nederlandse Orthopaedische Vereniging,

Anna Fonds, Universiteitsfonds Universiteit van Amsterdam, Department of Orthopaedic

Surgery AMC, DJO Global, Biomet, Arthrex, Smith& Nephew, Pro- Motion Orthopedics,

Bauerfeind Benelux B.V., Astra Tech Benelux B.V., Penders Voetzorg

ISBN 978-94-6169-210-8

Cover illustration:Maayke van Sterkenburg & Optima Grafische Communicatie

Layout and Printing: Optima Grafische Communicatie

Achilles tendinopathy

New insights in cause of pain, diagnosis and management

ACADEMISCH PROEFSCHRIFT

Ter verkrijging van de graad van doctor

aan de Universiteit van Amsterdam

op gezag van de Rector Magnificus

Prof. dr. D.C. van den Boom

ten overstaan van een door het college

voor promoties ingestelde commissie,

in het openbaar te verdedigen

in de Aula der Universiteit

op woensdag 4 april 2012, te 11:00 uur

door

Maayke Nadine van Sterkenburg

geboren te Leiderdorp

Promotiecommissie

Promotor Prof. dr. C.N. van Dijk

Copromotor Dr. G.M.M.J. Kerkhoffs

Overige leden Prof. dr. J.C. Goslings

Prof. dr. R.J. Oostra

Prof. dr. R.J.P.M. Scholten

Prof. dr. F.J.G. Backx

Prof. dr. R.L. Diercks

Dr. M. Maas

Faculteit der Geneeskunde

CONTENTS

PART I GENERAL INTRODUCTION 9

PART II TERMINOLOGY AND OUTCOME MEASURES 27

Chapter 1 Terminology for Achilles tendon related disorders CN van Dijk, MN van Sterkenburg, JI Wiegerinck, J Karlsson, N Maffulli. Knee Surgery Sports Traumatol Arthrosc 2011;19:835-841

29

Chapter 2 Outcome measures and assessment tools K Gravare Silbernagel, MN van Sterkenburg, A Brorsson, J Karlsson. Achilles tendinopathy:current concepts 2009:205-212

41

Chapter 3 Reliability and validity of the Dutch VISA-A questionnaire and applicability to non-athletes MN van Sterkenburg, IN Sierevelt, JL Tol, IV van Dalen, D Haverkamp, CN van Dijk. Submitted

53

PART III MIDPORTION ACHILLES TENDINOPATHY: CAUSE OF PAIN AND TREATMENT MODALITIES

67

Chapter 4 Less promising results with sclerosing Ethoxysclerol injections for Achilles tendinopathy: a retrospective study MN van Sterkenburg, MC de Jonge, IN Sierevelt, CN van Dijk. Am J Sports Med 2010; 38: 2226-2232

69

Chapter 5 Tendoskopie am Sprunggelenk und Fuß MN van Sterkenburg, PAJ de Leeuw, CN van Dijk. Artroskopie 2009; 22: 132-140

85

Chapter 6 The plantaris tendon and a potential role in midportion Achilles tendinopathy: an observational anatomical study MN van Sterkenburg, GMMJ Kerkhoffs, RP Kleipool, CN van Dijk. J Anat 2011; 218: 336-341

107

Chapter 7 Good outcome after stripping the plantaris tendon in patients with chronic midportion Achilles tendinopathy MN van Sterkenburg, GMMJ Kerkhoffs, CN van Dijk. Knee Surg Sports Traumatol Arthrosc 2011;19:1362-1366

121

Chapter 8 Midportion Achilles tendinopathy: why painful? An evidence based philosophy MN van Sterkenburg, CN van Dijk Knee Surg Sports Traumatol Arthrosc 2011;19:1367-1375

131

Part IV RETROCALCANEAL BURSITIS: DIAGNOSIS AND TREATMENT 149

Chapter 9 Appearance of the weight-bearing lateral radiograph in retrocalcaneal bursitis MN van Sterkenburg, B Muller, M Maas, IN Sierevelt, CN van Dijk. Acta Orthop 2010;81 387-390

151

Chapter 10 Endoscopic Calcaneoplasty Chapter in ‘Minimally invasive foot and ankle surgery’ MN van Sterkenburg, PAJ de Leeuw, CN van Dijk. Accepted for publication 2010

159

Chapter 11 Optimization of Portal Placement for Endoscopic Calcaneoplasty MN van Sterkenburg, M Groot, IN Sierevelt, GMMJ Kerkhoffs, CN van Dijk. Arthroscopy 2011;27:1110-1117

175

Part V GENERAL DISCUSSION 189

Part VI 207

SUMMARY 211

Samenvatting 221

Addendum 229

PArt iGeNerAL iNtroDUctioN

General introduction

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BAckGroUND

The Achilles tendon was weak, small or absent in the great ape, but is one of the hallmarks

of bipedal man. It possibly originated soon after the divergence of chimpanzee and human

lineages4. Its origination may be related to the greater relative length of the tarsal bones

in man. The name ‘Achilles tendon’ is derived from the Iliad by Homer. Achilles was made

invulnerable in infancy by his mother the goddess Thetis, who plunged him into the river

Styx. As he was held by one heel, this part was not bathed and so remained unprotected.

This heel was the site where Achilles was mortally wounded by a poisoned arrow launched

from the bow of Paris during the Trojan War. The ‘Achilles heel’ is currently used as an idiom

to express one’s principal weakness. In 1693 the Dutch surgeon Philip Verheyen changed the

concept ‘tendo magnus of Hippocrates’, the anatomical connection between the calcaneus

and triceps surae muscle, to ‘Achilles tendon’23.

The human body is built for movement. However, over the years we have become progres-

sively less active in daily life. The prevalence of obesity in the Western World has been rising,

and as a reaction keeping fit is increasingly advocated in recent years. Healthy nourishment,

physical discipline, and fitness occupy a considerable part of the cultural space. Endurance

sports like triathlons and long distance running have gained popularity. Although scientific

evidence supports the notion that humans evolved to be runners, with the ability to outrun

almost any animal when it comes to long distances28, overuse injuries have become promi-

nent in daily practice.

General inactivity during the week in an office-setting for many years, followed by

extreme and extensive exercise in the weekend without decent build-up in training program

allow for these types of injury to occur. Thirty to fifty percent of all sports injuries are due to

overuse, and overuse tendon injury has become an important issue in both recreational and

competitive athletes. Chronic Achilles tendon pathology is one of the most frequently occur-

ring problems in sports involving running and jumping. In elite long-distance runners there

even is a lifetime risk of 52% of sustaining an Achilles tendon injury24. However, the injury is

not always related to excessive physical activity. Thirty percent of patients have a sedentary

lifestyle, which may suggest that physical activity might exacerbate symptoms rather than

cause them3.

Recalcitrant Achilles tendons may cause pain for years and are often resistant to any form

of treatment. In the end, chronic Achilles tendon complaints may be self-limiting, since they

have been described to quench after an average of 8 years43. Doctors and athletes will not

consent with this prospect. Unfortunately, the cause of pain has not yet been clarified and

therefore its treatment is challenging and often unsatisfactory.

14

TerminologyThe terminology of chronic Achilles tendon disorders has been confusing. Maffulli and

co-workers proposed ‘Achilles tendinopathy’, the combination of Achilles tendon pain,

swelling, and impaired performance as standard terminology for chronic midportion prob-

lems, including the histopathological entities tendinosis and peritendinitis33. Terminology is

still confusing for problems around the insertion: retrocalcaneal bursitis, insertional spurs,

Haglund’s syndrome, - disease, - exostosis, pumpbump, cucumber heel and many more are

used interchangeably.

AnatomyThe Achilles tendon consists of the fibers of two muscle units in the superficial compartment

of the posterior leg: the gastrocnemius muscle (medial and lateral head) and the soleus

muscle. The gastrocnemius muscle crosses the knee and ankle joints (ankle and subtalar);

originating from the posterior surface of condylus medialis and -lateralis femoris and insert-

ing onto the calcaneus. The soleus muscle lies anterior to the gastrocnemius muscle and

originates from each side of the anterior aponeurosis attached to the tibia and fibula, and

from the posterior surfaces of the head of the fibula and its proximal quarter, as well as the

middle third of the medial border of the tibia. The soleus muscle only crosses the 2 ankle

joints. Distally, both the gastrocnemius and soleus muscles form an aponeurosis, from each

of which a tendon originates. At about the level where the soleus contributes fibers to the

Achilles tendon, rotation of the tendon begins and becomes more marked in the distal 5-6

cm. The gastrocnemius fibers rotate to lateral and the soleus fibers are positioned medial to

the insertion41. The Achilles tendon inserts crescent-shaped halfway the posterior tuberosity

of the calcaneus29. Just anterior to the distal portion of the Achilles tendon and posterior to

the posterosuperior calcaneal prominence the retrocalcaneal bursa is situated.

Unlike other tendons in the leg, the Achilles tendon lacks a synovial sheath. Instead, it

has a paratenon, which is an array of thin, fibrous tissue containing blood vessels49. Together

with the bone- tendon- and the muscle-tendon junction the paratenon forms the sole vas-

cular supply of the Achilles tendon. Within the paratenon, the plantaris tendon runs with

the Achilles tendon. The plantaris tendon is believed to be rudimentary. Absence in 7-20%

human lower limbs has been reported6, 7, 12, 39, 51.

The muscle of the plantaris muscle-tendon complex is triangularly shaped and lies poste-

rior to the knee joint, originating from the inferior part of the lateral supracondylar line of the

femur. The tendon travels inferomedially, posterior to the soleus muscle and anterior to the

medial gastrocnemius muscle. The tendon crosses the calf relatively proximal, running medial

from, and parallel with the Achilles tendon from the midportion of the calf; in the majority

of cases inserting medially onto the calcaneus7, 16. The plantaris tendon is considered to

function as a weak ankle- and knee flexor and ankle invertor.

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Clinical assessment of chronic Achilles tendon pathologyThe most common clinical diagnosis of chronic Achilles tendon problems is paratendinopathy

with or without tendinopathy (55-65%) (midportion tendinopathy), followed by insertional

problems such as retrocalcaneal bursitis and insertional spurs or calcifications (20-25%)17-19,

27. This thesis focuses on midportion Achilles tendinopathy and retrocalcaneal bursitis.

Midportion Achilles tendinopathy

General symptoms of midportion Achilles tendinopathy include painful swelling typically 2-7

centimeter (cm) proximal to the insertion, and stiffness especially when getting up after a

period of rest. Pain is often most prominent on the medial side of the tendon52.

Tendinopathy and paratendinopathy often co-exist. In isolated paratendinopathy, there is

local thickening of the paratenon. Paratendinopathy can be acute or chronic. Acute isolated

paratendinopathy manifests itself as peritendinous crepitation as the tendon tries to glide

within the inflamed covering. Areas of increased erythema, local heat, and palpable tendon

nodules or defects may also be present at clinical examination. In chronic Achilles paraten-

dinopathy, exercise-induced pain is still the cardinal symptom while crepitation and swelling

diminish. The area of swelling does not move with dorsiflexion and plantarflexion of the

ankle, where it does in tendinopathy35,55,60. In addition, ankle instability and malalignment

of the lower extremity, especially in the foot, should be looked for in patients with Achilles

tendon complaints.

Retrocalcaneal bursitis

Retrocalcaneal bursitis is caused by repetitive impingement of the bursa between Achilles

tendon and posterosuperior calcaneus. Differentiation between midportion and insertional

tendinopathy can be made on thorough history taking and physical examination. In case

of a retrocalcaneal bursitis, patients complain of pain after a day of strenuous activity or

when starting to walk after a period of rest. Wearing shoes with rigid heel counters is often

avoided. Physical examination reveals swelling on both sides of the Achilles tendon at the

level of the posterosuperior calcaneal prominence. Pain is aggravated by palpating this area

just medial and lateral to the Achilles tendon. Retrocalcaneal bursitis can be accompanied

by insertional tendinopathy. In case of insertional tendinopathy, there is pain at the bone-

tendon junction, which gets worse after exercise. The area of maximum tenderness is often

located in the central part of the insertion.

In clinical practice overuse injuries often do have features of more than one patho-

physiological entity, however in most cases thorough history taking and physical examination

should provide with the correct diagnosis.

16

ImagingStandard lateral and anteroposterior (AP) weight-bearing radiographs of the foot should

routinely be made even when soft tissue pathology is suspected, to exclude bony pathology

and assess foot deformities. Calcifications and bone spurs can be detected in case of inser-

tional tendinopathy. A posterosuperior calcaneal prominence can be seen and may cause

retrocalcaneal bursitis, but is not conclusive of the diagnosis. In case of a clinical diagnosis of

midportion tendinopathy or retrocalcaneal bursitis, additional investigations such as ultraso-

nography (US) or magnetic resonance imaging (MRI) can be helpful.

In midportion Achilles tendinopathy, US may reveal discontinuity of tendon fibers, focal

hypoechoic intratendinous areas, fusiform tendon swelling, and neovascularisation. In the

acute phase of paratendinopathy, there is fluid surrounding the tendon. Peritendinous adhe-

sions can be seen as thickening of the hypo-echoic paratenon with poorly defined borders.

In case of a retrocalcaneal bursitis fluid can be detected in the retrocalcaneal space, and an

insertional problem provides a hyperechoic signal.

US is a cost-effective and accurate measure to evaluate disorders of the Achilles tendon

and has the advantage of dynamic assessment, but is operator-dependent and often not

accessible by the orthopedic surgeon. Moreover, it is nowadays often superseded by contrast

enhanced MRI. Although MRI is expensive and time-consuming, its ability to acquire images

from multiple planes is an advantage, and is especially important for pre-operative planning.

The tendon proper may show expansion on T1- weighted images and central enhancement

of the signal within the tendon. In the acute phase of Achilles paratendinopathy, MRI is the

most useful imaging modality and shows high signal around the Achilles tendon on the STIR-

and T2 images. In the chronic phase the paratenon is thickened. In case of a retrocalcaneal

bursitis a high signal is seen on T2 and STIR in the retrocalcaneal space.

Outcome measuresMany studies have been published on different treatment modalities for Achilles tendinopathy.

Important in the evaluation of treatment outcome are standardized outcome measures46. A

patient’s subjective assessment of treatment outcome is increasingly appreciated. Criteria as

pain, functional ability and satisfaction fulfill the criteria of being valid, reliable and sensitive

to change if gathered by a correctly designed and tested patient-centered questionnaire8.

Response bias is minimized since the investigator has minimal influence on the scoring5, 56.

The Victorian Institute of Sports Assessment- Achilles (VISA-A) questionnaire was created

in 2001. It is a self- administered valid and reliable questionnaire evaluating symptoms and

their effect on physical activity46. Subjective scoring systems can be used in all countries after

translation and validation for specific language and population13, 14, 38.

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Management

Midportion tendinopathy

A wide range of conservative treatment measures is available for Achilles tendinopathy. An

eccentric training schedule is currently the treatment of first choice, preferably combined

with avoidance of painful activities, correction of malalignments of the foot, stretching and

use of NSAIDs when an acute element is present or just for pain relief. With compliance

this program is described to render good results in up to 90% of patients1,11,36,42,48,53. If it

fails, many other conservative measures can be applied, with varying results. An effective

treatment algorithm has not been developed yet. Independent of the levels of evidence, at 6

months after the start of treatment, 75-80% of patients report to be able to return to their

previous sporting activities. For the remaining patients surgical treatment can be considered.

Surgical measures can be divided into minimally invasive and open procedures, but also into

treatment for paratendinopathy, tendinopathy of the main body, and a combination of both.

Open debridement of the Achilles tendon is the most commonly performed procedure. After

removal of pathological tissue often enough tendon remains to achieve side-to-side closure.

When more than 50% of the tendon is degenerative, augmentation with a turn-down flap

and/or plantaris tendon can be performed, but larger defects require tendon transfer. When

the paratenon is involved, open adhesiolysis with or without resection of the paratenon can

be performed20,25,32,40,47. Aftertreatment for open debridement often consists of immobili-

zation in cast; modern postoperative strategies consist of bracing in walkers or the use of

heel raises and functional treatment. Return to sport tends to be at around the 6- month

mark but should be individualized. Because of the long time to recovery, minimally invasive

procedures have been developed to reduce per- and postoperative morbidity, rehabilitation

and time to normal activity. For isolated tendinopathy of the main body, percutaneous longi-

tudinal tenotomies can be performed34, 57; for paratendinopathy percutaneous stripping of

the paratenon and Achilles tendoscopy have been invented31, 55.

Success rates for the surgical management of non-insertional Achilles tendinopathy are

reported to be in the order of 75-100%26, 40, 44, 50. However, these results cannot be matched

with day-to-day clinical practice. These long-term difficulties in assessing the methods and

outcome of surgery are probably caused by a lack of understanding the pathology37.

Retrocalcaneal bursitis

Multiple conservative treatment options have been described to manage retrocalcaneal bur-

sitis, including avoidance of tight shoe heel counters, cast immobilization, NSAIDs, activity

modification, padding, shock wave treatment, physical therapy and injection of corticoste-

roids into the retrocalcaneal space. When these measures fail, surgical treatment can be

18

considered. Mostly open procedures performed through a lateral, medial or transverse Achil-

les tendon incision. The retrocalcaneal area is debrided and an osteotomy of the posterosu-

perior calcaneus is performed. These open procedures are invasive, have high complication

rates and rehabilitation is extensive7,20,31,32,42,47. Therefore, an endoscopic approach was

developed by Van Dijk et al.59. In this ‘endoscopic calcaneoplasty’ two portals are created,

just lateral and medial to the Achilles tendon, directly proximal to the superior part of the cal-

caneus. During the procedure, the retrocalcaneal bursa, posterosuperior calcaneus tuberosity

and local synovitis are addressed.

Current concepts on the cause of pain in midportion tendinopathyThe cause of complaints in midportion Achilles tendinopathy has not yet been unraveled;

however extensive research over the past three decades has led to the formulation of gener-

ally two different theories; (1) mechanical overuse and (2) neovascularisation. The first theory

hypothesizes that repetitive tensional loading with repeated strains below acute tendon injury

threshold induces microdamage. When matrix composition and organization is repaired and

mechanical strain continues on transiently weak tissue, tendon damage accumulates. Since

there is no time for proper repair due to overuse, degeneration develops. The poor vascu-

larisation and low metabolism contribute to the pathology. However, this theory does not

explain pain associated with tendinopathy, nor the cause of complaints in 30% of sedentary

patients45,54. Degeneration is believed to be associated with aging. Tendons become stiffer,

blood flow declines and responsiveness of cells to loading decreases45,54. Disuse is closely

connected to ageing; a disused tendon has similar changes as an aged tendon43. Neverthe-

less, degeneration does not seem to be an inevitable consequence of aging. Synergism of

overuse and ageing in the development of Achilles tendinopathy has been proposed54,58.

Several studies have reported intratendinous changes in up to 34% of cadaver specimens

and MRI images of patients without complaints10,15,21,22. A long-term follow-up study was

published by Alfredson et al. revealing persistent structural abnormalities and thickening

of the tendon 13 years after intratendinous surgery for Achilles tendinopathy, whereas all

patients were satisfied with the results and went back to Achilles tendon loading activities

without restrictions2. These studies imply that an area of intratendon abnormality of the

Achilles tendon proper is not necessarily the cause of pain.

The second, more recent theory on the cause of tendinopathy is the increased irregular

vascular and neurogenic ingrowth into the tendon proper as a contributory factor to the

pain in patients with symptomatic midportion tendinopathy. Pain-free normal tendons are

sparsely vascularised, which is even less at the two hypovascular regions at the insertion and

midportion area, commonly associated with pathology. Blood flow declines with ageing and

mechanical loading. Although the role of neovascularisation is poorly understood, and may

even be part of a healing response, treatment with Doppler ultrasound guided injection of

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Polidocanol (Ethoxysclerol) into these neovessels is described as a successful invasive conser-

vative treatment modality in different publications1-4,19,60.

Aims AND oUtLiNe of this thesis

This thesis aims at elucidating the cause of pain, and optimizing current diagnostic and

management methods in midportion Achilles tendinopathy and retrocalcaneal bursitis. A

better understanding will have positive consequences for the patients.

The terminology for chronic Achilles tendon pathology has become inconsistent and con-

fusing. Eponyms have been introduced but their definitions vary. Some terms represent a

disease, some an anatomic location, pathology, or a generic name. For proper research and

assessment of diagnosis and management, a uniform and clear terminology is necessary.

The objective of Chapter 1 is to provide a clear and uniform terminology for Achilles ten-

dinopathy. It comprises anatomic location, symptoms, clinical findings, and histopathology.

Chapter 2 reviews the currently available outcome measures and assessment tools for the

evaluation of complaints and outcome of interventions.

Validated outcome measures are essential in the evaluation of complaints and effective-

ness of treatment in both the clinical setting and research. The VISA-A has successfully been

translated into Swedish, German and Italian30, 38, 53. The aim of chapter 3 is to translate

and validate the Dutch version of the VISA-A subjective outcome measure for Achilles tendi-

nopathy (VISA-A-NL). It was hypothesized that the translated version would be a reliable and

valid tool in the subjective evaluation of complaints in patients with Achilles tendinopathy.

Another hypothesis was that the questions on activity could be deleted when applied to

non-athletes.

In Chapter 4 the aim was to evaluate the short- and midterm outcome of Ethoxysclerol

injections as a conservative measure for Achilles tendinopathy. This treatment was intro-

duced in 2003 by Alfredson et al. and was based on the findings of enhanced vascularisation

around degenerative tendons. Ethoxysclerol obliterates neovessels by destroying the intima

as is done in the treatment of varicose veins. We hypothesized that sclerosing Etoxysclerol

injections would not yield good results in the majority of patients.

When conservative measures fail, surgery can be considered. Also for operative interven-

tions many options are available. Minimally invasive treatment is preferable, and has proved

to cause less postoperative morbidity, to facilitate shorter rehabilitation and quicker sport

resumption when compared to open surgery. Amongst Achilles tendon endoscopy, ‘Achilles

tendoscopy’, chapter 5 describes the endoscopic approach and outcome of tendon prob-

lems around the ankle.

20

The exact pathophysiological mechanism causing midportion Achilles tendinopathy has not

yet been clarified. Obviously this is the main reason that the optimal treatment modality has

not yet been found. Pain is often located on the medial side of the Achilles tendon, where the

plantaris tendon accompanies the Achilles tendon. Also, most ultrasonographically detected

midportion disorders are found in the medial segment of the tendon9. In a healthy situation

the plantaris tendon is attached to the calcaneus or Achilles tendon at its insertion, but is

separate from the Achilles tendon at its midportion in 95%7. During Achilles tendoscopy it

is found that the plantaris tendon is fixed to the Achilles tendon at the level of complaints55.

The aim of chapter 6 is to evaluate the anatomic relations of the plantaris muscle and distal

tendon origins. We hypothesized that in chronic Achilles tendinopathy adhesions between

Achilles- and plantaris tendon are formed and so could seriously contribute to patient’s symp-

toms. In chapter 7 the results of stripping the plantaris tendon in 3 patients with midportion

Achilles tendinopathy are analyzed. It was hypothesized that stripping the plantaris tendon

would relate to a good outcome. In chapter 8, the cause of pain in midportion Achilles

tendinopathy is re-evaluated. We hypothesized that the tendon proper is not the cause of

complaints, but the process of scarring and adhesion of the paratenon onto the Achilles and

plantaris tendon that comes with the inflammatory response. This theory is elucidated using

the available evidence on the cause and treatment of midportion Achilles tendinopathy.

As described earlier, chronic Achilles tendon problems also occur around the tendon’s inser-

tion onto the calcaneus. Chronic retrocalcaneal bursitis is diagnosed at physical examination

as a prominent palpable swelling is palpable lateral and medial from the Achilles tendon just

proximal to the calcaneus. Standard lateral and anteroposterior radiographs of the ankle are

made to assess foot deformities or any bony abnormalities. In order to confirm the diagnosis

chronic retrocalcaneal bursitis, ultrasound, MRI or even bone scans are performed. These are

expensive and time consuming. Chapter 9 evaluates the usefulness of a visible soft tissue

swelling in the retrocalcaneal recess on standard lateral weight-bearing radiographs on the

ankle in diagnosing a retrocalcaneal bursitis. It was hypothesized that the retrocalcaneal

recess on radiography would be a useful and reliable tool in the diagnosis of a chronic

retrocalcaneal bursitis.

Primary treatment of choice consists of a number of conservative treatment options

including avoidance of tight shoe heel counters, cast immobilization, NSAIDs, activity modi-

fication, padding, shock wave treatment and physical therapy. When conservative treatment

fails, endoscopic calcaneoplasty can be performed. In chapter 10 this surgical procedure

is described. Adequately determining the location of landmarks can be difficult due to the

anatomy and swelling. Portals are positioned too far proximal and as a consequence the

posterosuperior part of the calcaneus cannot be reached properly resulting in a suboptimal

procedure or, when the problem is recognized, a need to re-incise or lengthen the incisions.

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For this reason, we aimed to standardize portal placement in chapter 11. It was hypothesized

that the landmark of the fibula tip in standard 2-portal hindfoot endoscopy was usable, and

that in patients with flat feet portals should be placed more proximal to this landmark.

22

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Heavy-load eccentric calf muscle training for

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2. Alfredson H, Zeisig E, Fahlstrom M. No

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3. Ames PR, Longo UG, Denaro V, Maffulli

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7. Daseler EH. The Plantaris Muscle: An Ana-

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JA, van Schie HT. Tendon Structure is Not

Related to Clinical Outcome Following

Eccentric Exercises in Chronic Mid-Portion

Achilles Tendinopathy. Unpublished results.

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R. Ultrasonographically detected changes

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24

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PArt ii termiNoLoGY AND

oUtcome meAsUres

Chapter 1

Terminology for Achilles tendon related disorders

Time for a change

CN van Dijk

MN van Sterkenburg

JI Wiegerinck

J Karlsson

N Maffulli

Knee Surgery Sports Traumatol Arthrosc 2011;19: 835-841

30

ABstrAct

The terminology of Achilles tendon pathology has become inconsistent and confusing

throughout the years. For proper research, assessment and treatment, a uniform and clear

terminology is necessary. A new terminology is proposed; the definitions hereof encompass

the anatomic location, symptoms, clinical findings and histopathology.

It comprises the following definitions: Midportion Achilles tendinopathy: a clinical

syndrome characterized by a combination of pain, swelling and impaired performance. It

includes, but is not limited to, the histopathological diagnosis of tendinosis. Achilles para-

tendinopathy: an acute or chronic inflammation and/or degeneration of the thin membrane

around the Achilles tendon. There are clear distinctions between acute paratendinopathy

and chronic paratendinopathy, both in symptoms as in histopathology. Insertional Achilles

tendinopathy: located at the insertion of the Achilles tendon onto the calcaneus, bone spurs

and calcifications in the tendon proper at the insertion site may exist. Retrocalcaneal bursitis:

an inflammation of the bursa in the recess between the anterior inferior side of the Achilles

tendon and the posterosuperior aspect of the calcaneus (retrocalcaneal recess). Superficial

calcaneal bursitis: inflammation of the bursa located between a calcaneal prominence or the

Achilles tendon and the skin.

Finally, it is suggested that previous terms as Haglund’s disease; Haglund’s syndrome;

Haglund’s deformity; pump bump (calcaneus altus; high prow heels; knobbly heels; cucum-

ber heel), are no longer used.

Ch

apter 1

Termin

olo

gy fo

r Ach

illes tend

on

related d

isord

ers

31

iNtroDUctioN

Overuse injuries of the Achilles tendon can be either insertional or non-insertional. As there

is no evidence available for chronic inflammation in patients with “tendinitis”, the term

tendinosis has been proposed instead1. In 1998, Maffulli et al. proposed to use the term

“tendinopathy” for the clinical syndrome characterized by a combination of pain, swelling

and impaired performance23. In Haglund’s syndrome, the pain is located at the postero-

superior calcaneal prominence. Originally, Haglund described pain in the hindfoot caused

by a prominent postero-superior corner of the calcaneus in combination with wearing a

rigid low-back shoe2,10. Today, when using the term Haglund’s exostosis, physicians are usu-

ally referring to a clinical situation of pain and tenderness at the postero-lateral aspect of

the calcaneus, where a calcaneal prominence can often be palpated. This is also known as

“pump-bump”, with alternative names as calcaneus altus, high prow heels, knobbly heels,

and cucumber heel.

A distinction between Haglund’s disease and other conditions such as a superficial Achilles

bursitis must be made. Haglund’s disease must be differentiated from Haglund’s syndrome,

which involves a painful swelling of an inflamed retrocalcaneal bursa, sometimes combined

with insertional tendinopathy of the Achilles tendon. It must also be distinguished from

Haglund’s disease, which is the term of osteochondrosis of the accessory navicular bone.

No doubt that all this is confusing: in reality, many different names and terms are used in

the literature. The purpose of this paper is to propose a terminology which includes the

combination of anatomic location, symptoms, clinical findings and pathological changes for

each entity.

historicAL PersPective

Midportion Achilles tendinopathy Philip Verheyen, a Dutch surgeon, was the first in 1693 to actually name the Achilles tendon

after the Greek hero Achilles16. Previously, it was known as “tendo magnus of Hippocrates”.

In 1883, Raynal described the first case of “cellulite peritendineuse of the Achilles tendon”32.

Other cases of “cellulite peritendineuse” of the Achilles tendon followed shortly2,17.

In 1905, Schanz was the first to describe a traumatic inflammation of the Achilles ten-

don: He described a patient who experienced ‘a chronic strain’ after mountain climbing36.

He entitled this “tendinitis Achillea traumatica”36. The inflammation was presumed to be

located in the Achilles tendon itself, instead of the insertion into the calcaneus, contrary to

the standard or ideas of the time1,34.

32

The terminology has changed more or less constantly, often without any evident scientific

reason throughout the 20th century. In 1950, Lipscomb proposed new definitions for inflam-

matory processes of tendons. He defined “paratendinitis” as an inflammatory process of

tendons or portions of tendons without a tendon sheath; “tenosynovitis” was implemented

to refer to inflammatory processes of tendons with a sheath. Additionally, he proposed

“peritendinitis” as a general term to refer to either “tenosynovitis” or “paratendinitis”20.

Since the 1970’s, increased effort was put in categorising Achilles tendon pathology, related

to subgroups. In 1976, Perugia et al. introduced new terminology on inflammatory problems

of the Achilles tendon30. They based their definitions on histological findings. Perugia et

al. differentiated between pure peritendinitis, peritendinitis associated with tendinosis, and

pure tendinosis. Peritendinitis was characterised by the presence of inflammation of the

peritendinous sheaths, without any pathological changes in the tendon itself. Peritendinitis

associated with tendinosis involved degenerative features of the tendon associated with

inflammation of the sheaths. Pure tendinosis was said to be characterized by degenerative

phenomena exclusively, often associated with foci of osteo-cartilaginous metaplasia. Later in

the same year, Puddu et al. published a paper clarifying the new terms introduced by Perugia

et al30,31. Tendinosis implied tendon degeneration, without any clinical or histological signs

of intratendinous inflammation.

Throughout the years, the discussion continued on the terminology of the location and on

the actual nomenclature of Achilles tendon disorders9,39. It took, however, until 1992 for

Clain and Baxter to divide the definitions of Achilles “tendinitis” in insertional and non-

insertional6.

In 1998, Maffulli et al.23 suggested to change the confusing terminology concerning overuse

tendon conditions. They proposed to use the terms “tendinosis”15, “paratendinitis”, and

“tendinitis” only after excision biopsy had been examined by a pathologist as these imply

specific, histopathologically proven conditions, with inflammatory cells23. They advised not

to use the aforementioned terms in clinical practice when discussing overuse tendon injuries.

The term “partial tear” should be reserved to acute partial tendinous lesions. In fact, this

term may be questioned altogether whether it does exist or not. “Achillodynia” is a purely

descriptive term, referring to pain in the region of the Achilles tendon1,24,34. Finally, Maf-

fulli et al. proposed to name the clinical syndrome of pain, swelling (diffuse or localised),

and impaired performance as tendinopathy. Depending on the involved tissues, the terms

tendinopathy, paratendinopathy, and pantendinopathy should be used23. Maffulli et al`s

publication has greatly helped to reduce the confusion in clinical terminology; the proposal

was broadly accepted, but it was not, however, implemented universally. Terminology has

therefore remained confusing27,40.

Ch

apter 1

Termin

olo

gy fo

r Ach

illes tend

on

related d

isord

ers

33

Pathology around the Achilles tendon insertionAlbert1 was the first to describe ‘Achillodynia’ in 1893, but the underlying pathology was

not determined, however25. In 1895, Rössler34 found that the cause of this Achillodynia

was an inflammation of the bursa between the insertion of the Achilles tendon and the

postero-superior tuberosity of the calcaneus. Three years later, Painter published his histo-

logical findings after resection of the post-calcaneal exostosis causing the inflammation of

the post-calcaneal bursa28. He concluded the exostoses were most probably manifestations

of an osteoarthritic process. In Patrick Haglund’s opinion, the term Achillodynia was too

general, and he divided patients into three groups: ‘Achillotendinitis ossificans’, ‘Bursitis

Achillea’, and children with growth problems of the epiphysis of the calcaneus. In terms

of “bursitis Achillea”, he noted there were 2 bursae: one located between the calcaneus

and the skin (bursa Achillea infero-posterior), and one between the Achilles tendon and

the calcaneus (bursa Achillea supero-anterior). In his opinion, the superficial bursitis was

caused by incorrect shoe-wear for ‘Kulturmenschen’ (culture people), and the other (deep

bursitis) by either acute or chronic trauma. The inferior posterior bursitis had, in his opinion,

no clinical relevance, but the superior anterior bursitis, caused by impingement between the

Achilles tendon and a bony prominence, on the calcaneus caused clinically relevant signs

and symptoms. This condition can be treated surgically by resecting the postero-superior

bony prominence of the calcaneus in case conservative measures fail10,28. In 1954, the term

‘pump bump’ arose. Dickinson et al. described the ‘pump bump’ as an enlargement of

the posterolateral aspect of the heel at the site of the insertion of the Achilles tendon and

Achilles tendon bursitis, mostly associated with wearing high heel shoes. When conservative

treatment failed, patients were treated surgically by excision of the posterosuperior corner

of the calcaneus7.

Until 1982, inflammation of the retro-calcaneal bursa caused by impingement between the

anterior aspect of the Achilles tendon and the posterior part of the calcaneus was named

retrocalcaneal bursitis. In that year, Pavlov et al. first described the ‘Haglund’s syndrome’,

defined as a frequent cause of posterior heel pain, characterized by a painful soft tissue

swelling at the level of the Achilles tendon insertion. Using a lateral heel radiograph, they

described a prominent calcaneal bursal projection, retro-calcaneal bursitis, thickening of the

Achilles tendon, and a convexity of the superficial soft tissues at the level of the Achilles

tendon insertion, a ‘pump bump’29. This is the first publication in which the authors used the

name ‘Haglund’. Haglund’s deformity was then described by Vega et al. as a tender swelling

in the region of the Achilles tendon with visible prominence of the postero-lateral aspect of

the calcaneus. In their opinion, the superficial Achilles bursa and/or the retrocalcaneal bursa

reflected the enlarged prominence. Then, in 1990 and 1991 ‘analogies’ for Haglund’s defor-

mity were described: Haglund’s syndrome, achillobursitis, achillodynia, and retro-calcaneal

bursitis were mentioned18,33. In 1993, Haglund’s disease was added to this list3, although

34

it was earlier described as being an osteochondrosis of the accessory navicular bone (or os

tibiale externum)5,18,42.

Sella et al.38 thought that all these names were confusing, and proposed separate definitions

for Haglund’s disease, Haglund’s syndrome, and Haglund’s deformity. Haglund’s disease was

referred to as osteochondrosis of the accessory navicular; Haglund’s deformity as a chronic,

sometimes painful distortion of the postero-superior and lateral portion of the calcaneus;

and the term Haglund’s syndrome was used when symptoms were present with/without the

deformity, and may involve the retro-calcaneal bursa as well as the Achilles tendon and the

superficial Achilles bursa38. This proposal was, however, not commonly adapted, and many

publications kept using terms interchangeably 4,11-13,19,21,22,26,37.

In 1998, the Federative Committee on Anatomical Terminology and the International

Federation of Associations of Anatomists published a general anatomic terminology8. This

“Terminologia Anatomica” defines the retrocalcaneal bursa as “bursa tendinis calcanei” and

the superficial calcaneal bursa is termed the “bursa subcutanea calcanea”8.

ProPoseD termiNoLoGY for AchiLLes teNDoN reLAteD DisorDers

Examining the evolution of the terminology over the years, the efforts and the struggle are

obvious. Some terms represent a disease, some an anatomic location, a pathology, or a

generic name. The reasoning behind a change in terminology is unclear; it appears largely

to be susceptible to fashion. In the 19th century, the terminology was mainly based on

anatomy1; later, it was based on histopathology30; others have proposed a ‘history’-based

terminology3,29,38.

Five leading anatomy journals were contacted, and asked for information on which terminol-

ogy they demanded from their authors. Based on the answers, it can be concluded that,

concerning anatomy, there is no such thing as a “standard terminology”. Some stated that

the authors were expected to use “widely accepted terminology”.

The definitions for Achilles tendon disorders should comprise anatomic location, symptoms,

clinical findings, and histopathology. The term to represent the entity must be neutral yet

descriptive, uniform and clear. The aforementioned lack of consistency should be avoided as

much as possible. The following definitions are therefore proposed (Table 1).

Ch

apter 1

Termin

olo

gy fo

r Ach

illes tend

on

related d

isord

ers

35

Tab

le 1

. Ter

min

olog

y fo

r A

chill

es t

endo

n re

late

d di

sord

ers,

incl

udin

g th

e an

atom

ic lo

catio

n, s

ympt

oms,

clin

ical

find

ings

his

topa

thol

ogy.

For

rad

iogr

aphi

c fin

ding

s,

see

tabl

e2

Term

An

ato

mic

loca

tio

nSy

mp

tom

sC

linic

al fi

nd

ing

sH

isto

pat

ho

log

y

Mid

po

rtio

n A

chill

es

ten

din

op

ath

y2-

7 cm

fro

m t

he in

sert

ion

onto

the

cal

cane

usA

com

bina

tion

of p

ain,

sw

ellin

g an

d im

paire

d pe

rfor

man

ce

Diff

use

or lo

caliz

ed

swel

ling

incl

udes

, but

is n

ot li

mite

d to

, the

his

topa

thol

ogic

al

diag

nosi

s of

ten

dino

sis:

impl

ies

hist

opat

holo

gica

l dia

gnos

is

of t

endo

n de

gene

ratio

n w

ithou

t cl

inic

al o

r hi

stol

ogic

al s

igns

of

intr

aten

dino

us in

flam

mat

ion,

not

nec

essa

rily

sym

ptom

atic

Para

ten

din

op

ath

yA

cute

Ch

ron

ic

arou

nd t

he m

id-p

ortio

n A

chill

es t

endo

n

arou

nd t

he m

id-p

ortio

n A

chill

es t

endo

n

Edem

a an

d hy

pere

mia

Exer

cise

-indu

ced

pain

palp

able

cre

pita

tions

, sw

ellin

g

crep

itatio

ns a

nd s

wel

ling

less

pro

noun

ced

edem

a an

d hy

pere

mia

of

para

teno

n, w

ith in

filtr

atio

n of

in

flam

mat

ory

cells

, pos

sibl

y w

ith p

rodu

ctio

n of

a fi

brin

ous

exsu

date

tha

t fil

ls t

he s

pace

bet

wee

n te

ndon

she

ath

and

tend

on.

para

teno

n th

icke

ned

as a

res

ult

of fi

brin

ous

exud

ate,

pr

omin

ent

and

wid

espr

ead

prol

ifera

tion

of (m

yo)fi

brob

last

s,

form

atio

n of

new

con

nect

ive

tissu

e an

d ad

hesi

ons

betw

een

tend

on, p

arat

enon

, and

cru

ral f

asci

a

Inse

rtio

nal

Ach

illes

te

nd

ino

pat

hy

inse

rtio

n of

Ach

illes

ten

don

onto

cal

cane

us, m

ost

ofte

n w

ith f

orm

atio

n of

bon

e sp

urs

and

calc

ifica

tions

in

tend

on p

rope

r at

inse

rtio

n si

te

Pain

, stif

fnes

s,

som

etim

es a

(sol

id)

swel

ling

Pain

ful t

endo

n in

sert

ion

at t

he m

id-p

ortio

n of

the

po

ster

ior

aspe

ct o

f th

e ca

lcan

eus,

sw

ellin

g m

ay

be v

isib

le a

nd a

bon

y sp

ur

may

be

palp

able

ossi

ficat

ion

of e

nthe

sial

fibr

ocar

tilag

e, a

nd s

omet

imes

sm

all

tend

on t

ears

occ

urrin

g at

ten

don-

bone

junc

tion

Ret

roca

lcan

eal b

urs

itis

Burs

a in

the

rec

ess

betw

een

the

ante

rior

infe

rior

side

of

the

Ach

illes

ten

don

and

the

post

eros

uper

ior

aspe

ct o

f th

e ca

lcan

eus

(ret

roca

lcan

eal r

eces

s)

Pain

ful s

wel

ling

supe

rior

to c

alca

neus

pa

infu

l sof

t tis

sue

swel

ling,

med

ial a

nd

late

ral t

o th

e A

chill

es

tend

on a

t th

e le

vel o

f th

e po

ster

osup

erio

r ca

lcan

eus

Fibr

o-ca

rtila

gino

us b

ursa

l wal

ls s

how

deg

ener

atio

n an

d/or

ca

lcifi

catio

n, w

ith h

yper

trop

hy o

f th

e sy

novi

al in

fold

ings

and

ac

cum

ulat

ion

of fl

uid

in t

he b

ursa

. A

ltern

ativ

ely,

the

bur

sa

may

be

prim

arily

invo

lved

by

infla

mm

ator

y or

infe

ctio

us

burs

itis

due

to a

n in

flam

mat

ory

arth

ropa

thy

Sup

erfi

cial

cal

can

eal

bu

rsit

isbu

rsa

loca

ted

betw

een

ca

lcan

eal p

rom

inen

ce o

r th

e A

chill

es t

endo

n an

d th

e sk

in

visi

ble,

pai

nful

, sol

id

swel

ling

post

erol

ater

al

calc

aneu

s (o

ften

as

soci

ated

with

sho

es

with

rig

id p

oste

rior

port

ion)

Vis

ible

, pai

nful

, sol

id

swel

ling

and

disc

olor

atio

n of

ski

n. M

ost

ofte

n lo

cate

d at

pos

tero

late

ral

calc

aneu

s; s

omet

imes

po

ster

ior

or p

oste

rom

edia

l

an a

cqui

red

adve

ntiti

ous

burs

a, d

evel

opin

g in

res

pons

e to

fric

tion.

Whe

n in

flam

ed, l

ined

by

hype

rtro

phic

syn

ovia

l tis

sue

and

fluid

.

36

Tab

le 2

. Rad

iolo

gic

findi

ngs

in A

chill

es t

endo

n di

sord

ers

Term

/Im

agin

gPl

ain

Radi

ogra

phy

Ultr

asou

ndC

TM

RI

Mid

po

rtio

n A

chill

es

ten

din

op

ath

yD

evia

tion

of s

oft

tissu

e co

ntou

rs is

usu

ally

pre

sent

. In

rar

e ca

ses

calc

ifica

tions

ca

n be

fou

nd

Tend

on la

rger

tha

n no

rmal

in b

oth

cros

s-se

ctio

nal a

rea

and

ante

ro-p

oste

rior

diam

eter

. H

ypoe

choi

c ar

eas

with

in t

he t

endo

n,

disr

uptio

n of

fibr

illar

pat

tern

, inc

reas

e in

te

ndon

vas

cula

rity

(Ech

o-D

oppl

er) m

ainl

y in

ve

ntra

l per

itend

inou

s ar

ea

In c

ase

(mas

sive

) cal

cific

atio

n ar

e se

en o

n pl

ain

radi

ogra

phy.

C

T im

agin

g ca

n be

hel

pful

in

pre

-ope

rativ

e pl

anni

ng,

show

ing

the

exac

t si

ze a

nd

loca

tion

of t

he c

alci

ficat

ions

Fat-

sat

urat

ed T

1 or

T2

imag

es: f

usifo

rm

expa

nsio

n ,c

entr

al

enha

ncem

ent

cons

iste

nt

with

intr

aten

dino

us

neov

ascu

lariz

atio

n

Para

ten

din

op

ath

yA

cute

Ch

ron

ic

-A

nor

mal

Ach

illes

ten

don

with

ci

rcum

fere

ntia

l hyp

oech

ogen

ic h

alo

A t

hick

ened

hyp

oech

oic

para

teno

n w

ith

poor

ly d

efine

d bo

rder

s m

ay s

how

as

a si

gn

of p

erite

ndin

ous

adhe

sion

s; in

crea

se in

te

ndon

vas

cula

rity

(Ech

o-D

oppl

er) m

ainl

y in

ve

ntra

l per

itend

inou

s ar

ea

-Pe

riphe

ral e

nhan

cem

ent

on

fat-

satu

rate

d T1

or

on T

2 im

ages

Inse

rtio

nal

Ach

illes

te

nd

ino

pat

hy

May

sho

w o

ssifi

catio

n or

a

bone

spu

r at

the

ten

don’

s in

sert

ion;

pos

sibl

y de

viat

ion

of s

oft

tissu

e co

ntou

rs

Cal

cane

al b

ony

abno

rmal

ities

Bone

for

mat

ion

at in

sert

ion.

CT

scan

is in

dica

ted

mai

nly

for

pre-

oper

ativ

e pl

anni

ng. I

t sh

ows

the

exac

t lo

catio

n an

d si

ze o

f th

e ca

lcifi

catio

ns a

nd s

purs

Bone

for

mat

ion

and/

or o

n ST

IR (s

hort

tau

inve

rsio

n re

cove

ry) h

yper

inte

nse

sign

al

at t

endo

n in

sert

ion

Ret

roca

lcan

eal b

urs

itis

A p

oste

rosu

perio

r ca

lcan

eal

prom

inen

ce c

an b

e id

entifi

ed; r

adio

-opa

city

of

the

retr

ocal

cane

al r

eces

s;

poss

ibly

dev

iatio

n of

sof

t tis

sue

cont

ours

Flui

d in

the

ret

roca

lcan

eal a

rea/

burs

a (h

yper

echo

ic)

-H

yper

inte

nse

sign

al in

re

troc

alca

neal

rec

ess

on T

2 w

eigh

ed im

ages

Sup

erfi

cial

cal

can

eal

bu

rsit

isPo

ssib

ly d

evia

tion

of s

oft

tissu

e co

ntou

rs

Flui

d be

twee

n sk

in a

nd A

chill

es t

endo

n-

Hyp

erin

tens

e si

gnal

bet

wee

n A

chill

es t

endo

n an

d su

bcut

aneo

us t

issu

e on

T2

wei

ghed

imag

es

Ch

apter 1

Termin

olo

gy fo

r Ach

illes tend

on

related d

isord

ers

37

Midportion Achilles tendinopathy Achilles tendinopathy is a clinical syndrome characterized by a combination of pain, swelling

and impaired performance. The swelling can be diffuse or localized. Typically, the nodular

swelling is located at 2-7 cm from the insertion onto the calcaneus. This part of the tendon

has also been described as the “main body of the Achilles tendon”. This entity involves

isolated pathology of the tendon proper, and includes, but is not limited to, the histopatho-

logical diagnosis of tendinosis23.

Tendinosis implies histopathological diagnosis of tendon degeneration without clinical

or histological signs of intratendinous inflammation, and is not necessarily symptomatic14.

However, it should be kept in mind that, although the histological term ‘tendinosis’ is also

widely used, the essential lesion of tendinopathy is not, strictu sensu, of a degenerative

nature: it has the features of a failed healing response, in which the tendon attempts to heal,

but, for some reason, including, possibly, continuous inappropriate mechanical stimuli, the

healing process appears non-finalised.

Achilles paratendinopathyParatendinopathy is defined by acute or chronic inflammation and/or degeneration of the

thin membrane around the Achilles tendon. Exercise-induced pain and local swelling around

the tendon’s midportion are the most important symptoms.

Histopathologically, acute paratendinopathy is characterized by edema and hyperemia of

the paratenon, with infiltration of inflammatory cells, possibly with production of a fibrinous

exsudate that fills the space between the tendon sheath and the tendon, causing palpable

crepitations on physical examination. In chronic Achilles paratendinopathy, exercise-induced

pain is the major symptom, while crepitations and swelling are less pronounced. Histopatho-

logically, the paratenon becomes thickened as a result of fibrinous exsudate, prominent and

widespread proliferation of (myo)fibroblasts, formation of new connective tissue and adhe-

sions between tendon, paratenon, and the crural fascia27.

Insertional Achilles tendinopathyInsertional Achilles tendinopathy is located at the insertion of the Achilles tendon onto the

calcaneus, possibly with the formation of bone spurs and calcifications in the tendon proper

at the insertion site. Patients complain of pain and stiffness and sometimes (a solid) swelling.

On physical examination, the tendon insertion (at the midportion of the posterior aspect of

the calcaneus) is painful. A swelling may be visible and a bony spur may be palpable. Histo-

pathologically, there is ossification of enthesial fibrocartilage, and sometimes small tendon

tears occurring at the tendon-bone junction35.

38

Retrocalcaneal bursitis An inflammation of the bursa in the recess between the anterior inferior side of the Achilles

tendon and the posterosuperior aspect of the calcaneus (retrocalcaneal recess) results in a

visible and painful soft tissue swelling, medial and lateral to the Achilles tendon at the level

of the posterosuperior calcaneus. Frequently, a posterosuperior calcaneal prominence can

be identified at plain radiography. Histopathologically, the fibro-cartilaginous bursal walls

show degeneration and/or calcification, with hypertrophy of the synovial infoldings and

accumulation of fluid in the bursa itself41. Alternatively, the bursa may be primarily involved

by inflammatory or infectious bursitis due to an inflammatory arthropathy.

Superficial calcaneal bursitis An inflammation of the bursa located between a calcaneal prominence or the Achilles ten-

don and the skin resulting in a visible, painful, solid swelling and discoloration of the skin. It

is most often located at the posterolateral aspect of the calcaneus. It is frequently associated

with shoes with a rigid posterior portion. The Achilles tendon is usually not involved, how-

ever. Histopathologically, the subcutaneous bursa is an adventitious bursa, which is acquired

after birth, and develops in response to friction. It is lined by hypertrophic synovial tissue and

fluid. A superficial calcaneal bursitis can be further specified by its location, i.e. posterior,

posterolateral, or posteromedial.

Achilles tendinopathy and paratendinopathy often co-exist. Retro-calcaneal bursitis is often

seen in combination with insertional tendinopathy. Other combinations are possible, but

occur less frequently.

coNcLUsioN

An inconsistent and erroneous change in nomenclature of disorders of the Achilles tendon

throughout the years has resulted in a large pool of confusing definitions and terms. A

uniform and clear terminology is necessary for proper research, diagnostics and treatment.

Proposed are new definitions, based on the anatomic location, symptoms, clinical findings

and histopathology. In addition it is proposed that Haglund’s disease, Haglund’s syndrome,

Haglund’s deformity, pump bump (calcaneus altus; high prow heels; knobbly heels; cucum-

ber heel), tendinitis are no longer used.

One of the following, depending on pathology, should be used instead: Midportion Achil-

les tendinopathy; Achilles paratendinopathy; insertional Achilles tendinopathy; retrocalcaneal

bursitis and superficial calcaneal bursitis.

Ch

apter 1

Termin

olo

gy fo

r Ach

illes tend

on

related d

isord

ers

39

refereNce List

1. Albert E. Achillodynie. Wien Med Presse

1893; 34: 41-43.

2. Baracz V. Tendonitis achillea arthritica als

eine besondere Form der Achillessehnener-

krankung. Zcntrafbt Chir 1906.

3. Biyani A, Jones DA. Results of excision of

calcaneal prominence. Acta Orthop Belg

1993; 59(1): 45-49.

4. Brunner J, Anderson J, O’Malley M, Bohne

W, Deland J, Kennedy J. Physician and

patient based outcomes following surgical

resection of Haglund’s deformity. Acta

Orthop Belg 2005; 71(6): 718-723.

5. Caffey J. Pediatric X-ray Diagnosis. 4th ed.

Chicago: Year Book Medical; 1962.

6. Clain MR, Baxter DE. Achilles tendinitis. Foot

Ankle 1992; 13(8): 482-487.

7. Dickinson PH, Coutts MB, Woodward EP,

Handler D. Tendo Achillis bursitis. Report

of twenty-one cases. J Bone Joint Surg Am

1966; 48(1): 77-81.

8. Federative Committee on Anatomical Termi-

nology. Terminologia Anatomica. Stuttgart-

New York: Thieme; 1998.

9. Fry HJH. Overuse Syndrome, alias Tenosy-

novitis/Tendinitis: The Terminological Hoax.

Plast Recons Surg 1986; 78(3): 414-417.

10. Haglund P. Beitrag zur Klinik der Achil-

lessehne. Zeitschr Orthop Chir 1928; 49:

49-58.

11. Harris CA, Peduto AJ. Achilles tendon imag-

ing. Australas Radiol 2006; 50(6): 513-525.

12. Jerosch J, Nasef NM. Endoscopic calcane-

oplasty--rationale, surgical technique, and

early results: a preliminary report. Knee Surg

Sports Traumatol Arthrosc 2003; 11(3): 190-

195.

13. Jerosch J, Schunck J, Sokkar SH. Endoscopic

calcaneoplasty (ECP) as a surgical treatment

of Haglund’s syndrome. Knee Surg Sports

Traumatol Arthrosc 2007; 15(7): 927-934.




Joint Surg Am 1991; 73(10): 1507-1525.

15. Khan KM, Bonar F, Desmond PM et al.

Patellar tendinosis (jumper’s knee): findings

at histopathologic examination, US, and MR

imaging. Victorian Institute of Sport Tendon

Study Group. Radiology 1996; 200(3): 821-

827.

16. Kirkup J. Mythology and History. In: Helal

B, Wilson D, editors. The Foot. Churchill

Livingstone; 1988: 1-8.

17. Kirmission. Cellulite peritendineuse du

tendon d’Achille. Arch Gen Med 1884; 1:

100-105.

18. Le TA, Joseph PM. Common exostectomies

of the rearfoot. Clin Podiatr Med Surg 1991;

8(3): 601-623.

19. Leitze Z, Sella EJ, Aversa JM. Endoscopic

decompression of the retrocalcaneal space.

J Bone Joint Surg Am 2003; 85-A(8): 1488-

1496.

20. Lipscomb PR. Tendons: Nonsuppurative

tenosynovitis and paratendinitis. Instr

Course Lect 1950; 7: 254-261.

21. Lohrer H, Nauck T, Dorn NV, Konerding MA.

Comparison of endoscopic and open resec-

tion for Haglund tuberosity in a cadaver

study. Foot Ankle Int 2006; 27(6): 445-450.

22. Ly JQ, Bui-Mansfield LT. Anatomy of and

abnormalities associated with Kager’s fat

Pad. AJR Am J Roentgenol 2004; 182(1):

147-154.




840-843.

24. Movin T, Kristoffersen-Wiberg M, Shalabi

A, Gad A, Aspelin P, Rolf C. Intratendinous

alterations as imaged by ultrasound and

contrast medium-enhanced magnetic reso-

nance in chronic achillodynia. Foot Ankle Int

1998; 19(5): 311-317.

40

25. Nielson AL. Diagnostic and Therapeutic

Point in Retrocalcanean Bursitis. J Am Med

Assoc 1921; 77(6): 463.

26. Ortmann FW, McBryde AM. Endoscopic

bony and soft-tissue decompression of

the retrocalcaneal space for the treatment

of Haglund deformity and retrocalcaneal

bursitis. Foot Ankle Int 2007; 28(2): 149-153.

27. Paavola M, Jarvinen TA. Paratendinopathy.

Foot Ankle Clin 2005; 10(2): 279-292.

28. Painter C.F. Inflammation of the post-

calcaneal bursa associated with exostosis. J

Bone Joint Surg Am 1898; s1-11: 169-180.

29. Pavlov H, Heneghan MA, Hersh A, Goldman

AB, Vigorita V. The Haglund syndrome:

initial and differential diagnosis. Radiology

1982; 144(1): 83-88.

30. Perugia L, Ippolitio E, Postacchini F. A new

approach to the pathology, clinical features

and treatment of stress tendinopathy of

the Achilles tendon. Ital J Orthop Traumatol

1976; 2(1): 5-21.

31. Puddu G, Ippolito E, Postacchini F. A clas-

sification of Achilles tendon disease. Am J

Sports Med 1976; 4(4): 145-150.

32. Raynal E. Cellulite peritendineuse du tendon

d’Achille. Arch Gen Med 1883; 11(2): 677-

689.

33. Reinherz RP, Smith BA, Henning KE.

Understanding the pathologic Haglund’s

deformity. J Foot Surg 1990; 29(5): 432-435.

34. Rössler. Zur Kenntniss der Achillodynie.

Deutsch Ztschr f Chir 1895; 52: 274-291.

35. Rufai A, Ralphs JR, Benjamin M. Structure

and histopathology of the insertional region

of the human Achilles tendon. J Orthop Res

1995; 13(4): 585-593.

36. Schanz A. Eine typische Erkrankung der

Achillessehne. Zentralblatt für Chirurgie

1905; 32: 1289-1291.

37. Schunck J, Jerosch J. Operative treatment

of Haglund’s syndrome. Basics, indications,

procedures, surgical techniques, results and

problems. Foot Ankle Surg 2005; 11: 123-

130.

38. Sella EJ, Caminear DS, McLarney EA.

Haglund’s Syndrome. J Foot Ankle Surg

1997; 37(2): 110-114.

39. Smith DC. Tendinitis- or peri tendinitis. Brit

Med J 1960; 5183: 1429.

40. Sorosky B, Press J, Plastaras C, Rittenberg

J. The practical management of Achilles

tendinopathy. Clin J Sport Med 2004; 14(1):

40-44.

41. Stephens MM. Haglund’s deformity and

retrocalcaneal bursitis. Orthop Clin North

Am 1994; 25(1): 41-46.

42. Vega MR, Cavolo DJ, Green RM, Cohen RS.

Haglund’s deformity. J Am Podiatry Assoc

1984; 74(3): 129-135.

Chapter 2

Outcome measures and assessment tools

K Grävare Silbernagel

MN van Sterkenburg

A Brorsson

J Karlsson

Achilles tendinopathy: current concepts 2009: 205-212

42

iNtroDUctioN

Tallon and co-workers75 published a review of the outcome after surgery in patients with

chronic Achilles tendinopathy and pointed at the deficiencies in outcome assessment and

criteria. They recommended the use of outcome measures that were condition-specific, reli-

able, sensitive, and correlated with clinical severity.

oUtcome scores – qUestioNNAires

Many research studies have not used specific outcome measures validated for Achilles tendi-

nopathy. Instead, many studies use patient-reported pain (on a Visual Analogue Scale) with

tendon loading activity as a main outcome measure to determine the success of treatment.

Sometimes, the investigators have graded the success of treatment based on patient-reported

improvements1,41,45,51,76.

To minimize the response bias, which can affect the patients’ reports of pain and symp-

toms, it is important to use outcome assessments in which the investigator has a minimal

influence on the scoring12,75. In many of the above-mentioned studies, it is difficult to judge

how much the investigator could have influenced the results. Many studies include question-

naires relating to symptoms, physical activity, other treatments and previous injuries, but they

are rarely specific standardized questionnaires. The lack of standardized outcome measures

for Achilles tendinopathy caused previously difficulties when comparing treatment studies75.

A performance test protocol and scoring scale for the evaluation of ankle injuries by Kaik-

konen and co-workers has been used in a follow-up study of patients with Achilles tendi-

nopathy25,49,50. It includes both objective and subjective measurements and has been shown

to have good reliability in healthy individuals and to be able to distinguish patients with

ankle ligament injury from healthy individuals. However, its validity on patients with Achilles

tendinopathy has not been evaluated.

Stanish and co-workers73 designed a system for tendon symptom classification (Table 1). This

classification system has not been evaluated for reliability and validity, but it has been used

as an outcome measure after surgery in patients with ‘achillodynia’56.

The VISA-A questionnaireIn 2001, Robinson and co-workers55 developed a questionnaire as an index of the clinical

severity of Achilles tendinopathy, the Victorian Institute of Sports Assessment – Achilles

questionnaire (VISA-A). This questionnaire is based on a similar questionnaire for patellar

tendinopathy79,80. The VISA-A questionnaire is the first outcome measure designed specifi-

cally for Achilles tendinopathy. It has also been evaluated and shown to have good reliability

Ch

apter 2

Ou

tcom

e measu

res and

assessmen

t too

ls

43and validity38,55,72. A factor analysis of the Swedish version of the VISA-A questionnaire

(VISA-A-S) revealed that the questionnaire evaluated the two factors pain/symptoms and

physical activity72. The VISA-A-S questionnaire also has been shown to have a large effect

size indicating that it is responsive to clinically relevant changes71. The high responsiveness

(as indicated by an effect size of 2.1) also indicates that the VISA-A-S questionnaire can be

useful as an outcome measure in scientific studies.

When reviewing the literature we found that the VISA-A questionnaire had been used

as an outcome measure in 19 studies on treatment for patients with Achilles tendinopa-

thy9-11,15-17,39, 40, 53, 54, 57-59,65,69-71,77,78. Furthermore, the VISA-A questionnaire had been

translated to Italian and Swedish, and these versions were also shown to be reliable and

valid38,72.

The VISA-A is a self-administered questionnaire and provides an index of the clinical sever-

ity, which is easily followed over time, for patients with Achilles tendinopathy. The score

ranges between 0-100, and a lower score indicates worse symptoms and greater limitation

on physical activity. It can be used to compare different populations with Achilles tendinopa-

thy and to facilitate comparisons between studies. In the clinic, the VISA-A questionnaire can

be used to assess the clinical severity of the patient’s symptoms and provide a guideline for

treatment, as well as for monitoring the effect of treatment. This score might be less valid for

sedentary persons suffering from Achilles tendinopathy.

The Foot and Ankle Outcome ScoreThe Foot and Ankle Outcome Score (FAOS) is a questionnaire that assesses patients’ symp-

toms, function and foot- and ankle-related quality of life60. The FAOS content is based on

the Knee injury and Osteoarthritis Outcome Score (KOOS) and has been shown to have

good content validity and reliability in patients with ankle injury60. It has, however, not been

validated for patients with Achilles tendinopathy. When used as an outcome measure for

patients with Achilles tendinopathy, it has been shown to be responsive to changes over time

with treatment 60,28,61.

Table 1. Classification system for the effect of pain on athletic performance (Stanish et al 2000)

Level Description of pain Level of sports performance

1 No pain Normal

2 Pain only with extreme exertion Normal

3 Pain with extreme exertion and 1 to 2 hours afterwards Normal or slightly decreased

4 Pain during and after vigorous activities Somewhat decreased

5 Pain during activity and forcing termination Markedly decreased

6 Pain during daily activities Unable to perform

44

fUNctioNAL AssessmeNt

Achilles tendinopathy appears to cause difficulties with physical activities in the active

population, but exactly how it affects the lower leg muscle-tendon functions is not fully

understood69. Muscular strength, power, muscular endurance, flexibility and motor control

are important in physical performance. The improvements of these factors are therefore

often prescribed in rehabilitation and injury prevention programs for tendon injuries 14,73.

StrengthStrength measurements with dynamometry have been performed in patients with Achilles

tendinopathy, in both etiological and prospective treatment studies1,2,21,42,45,50,76.

Isokinetic dynamometry has been used to test ankle plantarflexion and dorsiflexion

strength both concentrically and eccentrically at various angular velocities such as 30o/s,

50o/s, 60o/s, 120o/s, 180o/s, and 225o/s1,2,21,42,45. Paavola and co-workers50, on the other

hand, measured the isometric strength of the lower limb in an isometric leg press dyna-

mometer. Testa and co-workers76 measured maximum isometric muscle activation, as well as

isometric muscular endurance, in patients with Achilles tendinopathy.

The various body positions described in the literature and used in the clinical setting to

measure plantarflexion and dorsiflexion strength are supine with the knee and hip extended,

sitting with the hip in 100-110 degrees of flexion and the knee in either 40 degrees or 90

degrees of flexion and a closed-chain position in which the measurement pad was placed

on the knee1,2,21,42,43,45. The reliability of isokinetic and isometric dynamometry is generally

high, and the various testing positions for plantarflexion and dorsiflexion have good test-

retest reliability2,43. A test for measuring muscular strength and power of the ankle plan-

tarflexion in a regular weight-training machine has also been shown to be reliable and valid

for patients with Achilles tendinopathy69. In this test, muscle power development, i.e. the

ability to produce a high force quickly, was evaluated both concentrically and eccentrically-

concentrically. The reason for evaluating muscle power was because power is considered to

be more important for both sports performance and injury protection, than the ability to

produce a high force31. Patients with Achilles tendinopathy had a significant deficit on their

injured side (or most symptomatic side) compared with their uninjured (or least symptomatic

side) in both concentric and eccentric-concentric plantarflexion while standing69.

It is, however, important to remember that strength tests are valid for measuring improve-

ments in strength, but they are only moderately correlated to functional performance and

need to be complemented with other types of functional assessment4.

Endurance testMuscular endurance testing is another type of muscle function measurement. In a heel-rise

test (also called heel-raise, heel-drop or toe-raise), repetitive plantarflexion of the ankle is

Ch

apter 2

Ou

tcom

e measu

res and

assessmen

t too

ls

45

performed on standing until fatigued. It is the most commonly used test for measuring the

muscular endurance of the calf musculature. The normal number of heel-rise repetitions

on one healthy leg is regarded to be approximately 25, but it can range from six to 70

in healthy individuals 35. The testing position for the subject is standing on one leg while

maintaining a straight knee, support with the fingertips for balance and avoiding body sway

forward. This test has been used in several research studies and has shown good reliability

(ICC 0.78-0.84) 43,74. The heel-rise test has been used in evaluations of patients with Achilles

tendon ruptures, as part of a scoring scale used for patients with Achilles tendinopathy

and in prospective studies of Achilles tendinopathy44,49,50. Even though heel-rises are often

prescribed during the rehabilitation of Achilles tendinopathy, they are not commonly used to

evaluate the effect of treatment. One study found no significant deficit on their injured side

(or most symptomatic side) compared with their uninjured (or least symptomatic side) on

the toe-raise test69. Since the treatment for Achilles tendinopathy include toe-raises, the test

is useful to evaluate the effect of treatment and improvements in heel-rise endurance with

treatment has been found in patients with Achilles tendinopathy70.

Jump testsVarious jump tests are often used to evaluate function in patients with lower extremity

injuries, as well as to evaluate functional performance in athletes18,47,83. High loads occur on

the Achilles tendon during activities during which the so-called stretch-shortening cycle (SSC)

is utilized20,30. The SSC is a combination of an eccentric muscle action (with lengthening of

the muscle and tendon) immediately followed by a concentric muscle action (shortening

of the muscle-tendon complex)8,29. The concentric force production will be higher when

preceded by an eccentric muscle action compared with a pure concentric muscle action8,29.

The efficiency of utilizing the SSC in various types of jumps reportedly ranges from 17-34% 5,20. Achilles tendon elasticity is important to store and release energy during the SSC, and

thereby improves the economy and performance of motion20,29. Changes in lower leg

functions such as muscle-tendon strength, endurance, flexibility and motor control could all

affect the various mechanisms in the SSC, and these changes might be etiological factors for

the development of Achilles tendinopathy21,74.

Jump tests such as counter-movement jumps (CMJ), squat jump (SJ) and hopping have

been used to evaluate the loading of the Achilles tendon30. CMJ and SJ are vertical jumps

where the jump height is used for evaluation. In the CMJ, the starting position is upright

whereas for the SJ the starting position is with the knees bent. Hopping is a continuous

rhythmical jump, similar to jumping rope and here the contact times and flight times are

usually evaluated 20,30. A drop counter-movement jump (Drop CMJ) is performed jumping

down from a box/step and directly on landing performing maximal vertical jump. This type

of jump is often used in training to improve jumping ability in athletes and it also places high

46

demands on the ability to utilize the SSC. One study on patients with Achilles tendinopathy

found significant deficit in hopping and Drop CMJ on their injured side (or most symptomatic

side) compared to their uninjured (or least symptomatic side) but this was not found on the

CMJ69,70. Another often used jump test is the one-legged hop for distance and it has also

been used in a prospective study to identify intrinsic risk factors for Achilles tendon overuse

injury42. Even though Achilles tendinopathy is thought to be related to running and jumping,

there are only a few prospective treatment studies that have evaluated the patient’s recovery

in terms of jumping ability.

coNcLUsioN

Thorough history taking and clinical examination are essential in diagnosing Achilles tendi-

nopathy. Although our findings suggest that imaging adds little information of use for expert

sports medicine clinicians in diagnosing tendinopathy, it is useful in preoperative planning

and possibly for less experienced clinicians, who are unsure of their diagnoses and unfamiliar

with subjective outcome measures.

Achilles tendinopathy causes not only pain, symptoms and difficulty with physical activity

but also impairments in various aspects of lower leg function. It is therefore important to

continuously evaluate the patients’ progress with both validated subjective scoring systems,

such as the VISA-A questionnaire, and with various validated functional tests. Also the

patients’ reported subjective pain and ability to return to previous physical activity and sports

are important outcome measures. Proper evaluations with validated tests are not only for

scientific purposes, but also of importance to the practitioner and the patient to follow the

progress with treatment and rehabilitation.

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Chapter 3

Reliability and validity of the Dutch VISA-A questionnaire

for Achilles tendinopathy and applicability to non-athletes

MN van Sterkenburg

IN Sierevelt

JL Tol

IV van Dalen

D Haverkamp

CN van Dijk

Submitted

54

ABstrAct

BackgroundIn 2001, the Victorian Institute of Sports Assessment developed a self-administered question-

naire evaluating symptoms and their effect on physical activity for patients with Achilles

tendinopathy. It has proven to be an effective outcome questionnaire in various languages.

The aim of this project is to translate and validate the VISA-A questionnaire into the Dutch

language (VISA-A-NL) and to assess its applicability to non-athletes.

MethodsAfter translation according to a forward-backward protocol, 101 patients with complaints of

Achilles tendinopathy were asked to fill out the VISA-A-NL at two time points together with

VAS, FAOS and SF-36 questionnaires. Reliability, internal consistency, construct- and content

validity were tested.

ResultsThe VISA-A-NL showed high reliability (0.97 (95% CI 0.95-0.98)). Crohnbach’s alpha (internal

consistency) was 0.80. It increased to 0.88 without activity domain. Correlation with other

questionnaires was moderate or poorer.

ConclusionThe VISA-A-NL proved to be an excellent evaluation instrument for the Dutch physician. If

applied to non-athletes, using a modified score (questions 1-6) should be considered.

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iNtroDUctioN

Achilles tendinopathy is a major cause of chronic pain and disability. This may lead to sub-

optimal overall health as physical inactivity is a risk factor for cardiovascular disease16. Many

studies have been published on a magnitude of treatments for Achilles tendinopathy, but

prospective series on the outcome are lacking. One of the factors limiting the quality of

research may be the absence of standardised outcome measures to evaluate the outcome of

treatment19. A patient’s subjective assessment of treatment outcome such as pain, functional

ability and satisfaction fulfils the criteria of being valid, reliable and sensitive to change if

gathered by a correctly designed and tested patient-centred questionnaire6. The Victorian

Institute of Sports Assessment- Achilles (VISA-A) questionnaire was created in 2001 to assess

clinical severity for patients with Achilles tendinopathy. It is a self- administered question-

naire evaluating symptoms and their effect on physical activity19, and displayed reliability

and construct validity. Subjective scoring systems can be used in countries other than the

ones in which they were developed if translated and validated for a specific language and

population10,11,17. The VISA-A has been translated into Swedish, Italian, and German and

proved to be able to determine the clinical severity and provide information about the effect

of the management of patients with Achilles tendinopathy in these languages15,16,21. The

aim of this project is to translate and validate the VISA-A questionnaire into the Dutch

language (VISA-A-NL) to provide a valid questionnaire for the Dutch population. Moreover,

the questionnaire seems to be designed only for athletes as 40% of the points account for

activity. As approximately 30% of patients with complaints of Achilles tendinopathy have a

sedentary lifestyle2, applicability to non-athletes is also evaluated.

methoDs

Translation procedure A Dutch translation was made using a forward-backward translation protocol according to

the guidelines of Guillemin and co-workers10,11. Three people independently translated the

English version of the VISA-A questionnaire to Dutch. All three were in the medical field, and

had English as a second language. One independent native speaker, not active in the medi-

cal field translated this Dutch version back into English. Discrepancies were discussed and

adjusted for the final Dutch questionnaire (VISA-A-NL, see addendum). It was assumed that

no major cultural differences in lifestyle exist between the Dutch and Canadian population,

and that therefore cultural adaptation of the questionnaire was not required 3,10.

56

Patients104 consecutive patients were included from the outpatient clinic of 3 participating Dutch

hospitals of whom 47% were female. Mean age was 48.5 years (SD 11.6), 79 (76%) patients

were athletes, 25 (24%) were non-athletes.

All patients had complaints of Achilles tendinopathy (including midportion- and inser-

tional tendinopathy, paratendinopathy and retrocalcaneal bursitis)25.

They were clinically assessed and an AOFAS was taken by the consulting physician. All

patients were asked to fill out 2 sets of questionnaires; the first (A= VISA-A-NL, VAS pain,

VAS function, FAOS, SF-36) at the day of consultation, the second (B= VISA-A-NL) they were

to complete 4-5 days later24. Additionally they were asked whether their complaints had

changed since the first assessment.

QuestionnairesThe original English version of the VISA-A questionnaire as designed by Robinson and co-

workers19 contains eight questions that cover three domains; pain (questions 1-3), function

(questions 4-6), and activity (questions 7-8). Scores are summed to yield a total of 100 points

in an asymptomatic subject: questions 1-7 score a maximum of 10 points each; question 8,

on sporting activity, carries a maximum of 30. Pain on undertaking sports will automatically

lead to a loss of 10-20 points.

Since question 7 and 8 refer to sport activities (accounting for 40% of points) and the

study population contained both athletes and non-athletes, we modified the VISA-A score

by deleting both questions and investigated the psychometric properties of both the VISA

and the modified VISA.

The FAOS is a 42-item questionnaire divided into 5 subscales: pain (9 items), other symp-

toms (7 items), activities of daily living (17 items), sport and recreation function (5 items), foot

and ankle related quality of life (4 items). Each question can be scored on a 5-point Likert

scale (0-4) and each of the five subscale scores is calculated as the sum of the items included.

Raw scores are then transformed to a 0-100, worst to best score20.

The SF-36 is a self-administered, generic HRQL (health related quality of life) instru-

ment1,5,23,26. It comprises 36 items across 8 dimensions (physical functioning, role limitation

due to physical problems, bodily pain, perception of general health, energy and vitality, social

functioning, role limitation due to emotional problems, and mental health). The 8 dimen-

sions of the SF-36 score are calculated on a 0-100 worst to best scale13.

The VAS is a 100 mm visual analogue scale and is used to determine the seriousness of

pain and functional problems18.

In 1994 the American Orthopaedic Foot and Ankle Society (AOFAS) developed a question-

naire to provide a standard method for reporting clinical status of the ankle and foot. The

AOFAS- ankle and hindfoot clinical rating system combines both subjective and objective fac-

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tors into numerical scales to describe function, alignment and pain. Since objective aspects

are incorporated, this questionnaire has to be completed by the investigator14.

TestingWhen a questionnaire is developed or translated, the most important consideration is that it

must be able to accurately measure that for which it is designed. To evaluate the psychomet-

ric properties of the VISA-A-NL, both reliability and validity were assessed.

Reliability

Reliability is defined as the extent to which patients can be distinguished from each other,

despite measurement errors22.

Test-retest reliability refers to the repeatability of the test and measures the extent to

which the same results are obtained on repeated administration when no change in physical

functioning has occurred8. To determine the test-retest reliability, a second VISA-A-NL (B)

questionnaire was given to all patients; 67 patients responded. In 15 patients, complaints

had changed at re-test. Test-retest reliability was therefore assessed in 52 patients, using

the intra-class coefficient (ICCagreement, two-way random effects model). An ICC >0.75 was

considered good9. A t-test was performed to determine the presence of a systematic differ-

ence between the first and second assessment. Additionally, Standard Error of Measurement

(SEM) was calculated as the square root of the within subject variance. The Smallest Detect-

able Change (SDC) was calculated as 1.96 x √2 x SEM. The SDC is the smallest measurement

change that can be interpreted as real change4.

Internal consistency of the scale is the extent to which the items are inter-correlated and

cover the same construct (homogeneity of the scale). To evaluate the internal consistency of

the VISA-A Cronbach’s alpha was calculated. A Crohnbach’s alpha of 0.7 was considered to

represent an acceptable degree of internal consistency, 0.8 was considered as good and 0.9

as excellent internal consistency7.

Validity

Validity relates to the ability of a questionnaire to measure to outcome parameter of interest.

Construct validity was tested by determining the association between the VISA-A-NL

questionnaire and the FAOS, SF-36, VAS-scores for pain and function, and the AOFAS, using

Pearson correlation coefficients. We evaluated convergent and divergent validity by hypoth-

esizing that correlation coefficients between the VISA-A-NL (with and without the activity

questions) and VAS pain, FAOS pain, -symptoms, -sport and recreation and SF-36 bodily pain

and physical functioning would be higher than correlations with the other domains.

Content validity examines the extent to which all concepts of interest are adequately

represented by the items in the questionnaire24. It was evaluated by assessing distribution

58

and floor and ceiling effects of the VISA-A-NL. These are considered to be present if more

than 15% of responders achieve the lowest or highest possible score24.

Statistics

Statistical analysis was performed using PASW statistics 18.0 software (SPSS Inc., Chicago,

IL). A p-value of less than 0.05 was considered statistically significant.

resULts

Of 104 participans, 11 questionnaires were filled out incompletely or erroneously and there-

fore excluded from analysis (n=93).

ReliabilityOf 93 patients, 52 (56%) returned the second set of questionnaires. The ICCagreement of

the questionnaire was 0.97 (95% CI: 0.95-0.98) and Crohnbach’s alpha was 0.78 for the

entire study population (table 1). A statistically significant difference between the two assess-

ments was not observed for both versions of the VISA-A-NL in athletes nor in non-athletes

(0.29<p<0.67).

Table 1. Results

Athletes (n=39) Non-athletes (n=13) Total (n=52)

ICC VISA total (95%CI)

0.95 (0.91-0.97) - 0.97 (0.95-0.98)

ICC VISA modified(95%CI)

0.96 (0.92-0.98) 0.98 (0.93-0.99) 0.97 (0.95-0.98)

SEM VISA total 4.41 (4.4%) - 4.07 (4.1%)

SEM VISA modified 2,64 (4.4%) 2,42 (4.0%) 2,68 (4.5%)

SDC VISA total 12,21 (12.2%) - 11,28 (11.3%)

SDC VISA modified 7,32 (12.2%) 6,70 (11.2%) 7,44 (12.4%)

ICC= Intra Class Correlation coefficient, SEM = Standard Error of Measurement, SDC = smallest detect-able change

Athletes (n=71) Non-athletes (n=22) Total (n=93)

Crohbach’s Alpha VISA total 0.72 0.82 0.78

Crohbach’s Alpha VISA

modified

0.83 0.86 0.86

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ValidityPearson correlation coefficients of the VISA-A-NL with the other questionnaires are shown in

table 2. The subscale ‘SF-36 physical functioning’ correlated well with the VISA-A-NL ques-

tionnaire, both with and without activity domain. Most other physical domains correlated

moderately but, the subscales of FAOS quality of life showed poor correlation with VISA-A.

Poor correlation was also observed for the psychological domains (SF-36 social functioning,

mental health, role emotional, vitality, general health perception).

The mean scores of the VISA-A-NL questionnaire was 52.4 (SD 19.7) and 22.0 (SD 15.7) for

athletes and non-athletes, respectively. The mean scores of the modified VISA-A-NL question-

naire was 36.2 (SD 13.9) and again 22.0 (SD 15.7) for athletes and non-athletes, respectively.

Table 2. Pearson correlation coefficients of the VISA-A-NL with the other questionnaires of subject (with and without activity domain). * p<0.05

VISA-A TotalAthletes (n=71)

VISA-AModifiedAthletes (n=71)

VISA-AModifiedNon-athletes (n=22)

VISA-A Totalentire population (n=93)

VISA-AModifiedentire population (n=93)

VAS Pain -0.54* -0.58* -0.39 -0.54* -0.57*

VAS Function 0.52* 0.51* 0.44* 0.50* 0.52*

AOFAS 0.48* 0.46* 0.31 0.56* 0.50*

FAOS Symptoms 0.45* 0.52* 0.53* 0.58* 0.60*

FAOS Pain 0.53* 0.56* 0.52* 0.58* 0.60*

FAOS ADL 0.56* 0.55* 0.47* 0.59* 0.58*

FAOS Sport 0.56* 0.61* 0.43* 0.55* 0.59*

FAOS QOL 0.29* 0.33* 0.14 0.38* 0.37*

SF -36 Physical functioning

0.55* 0.63* 0.66* 0.70* 0.71*

SF-36 Role physical 0.13 0.12 0.58* 0.31* 0.32*

SF-36 Bodily pain 0.31 0.40* 0.46* 0.49* 0.51*

SF-36 Social functioning 0.01 -0.04 0.29 0.27* 0.21

SF-36 Mental health -0.11 -0.07 0.39 0.21 0.20

SF-36 Role emotional -0.06 0.02 0.65* 0.37* 0.39*

SF-36 Vitality -0.26 -0.25 0.26 -0.05 -0.09

SF-36 General health perception

-0.01 -0.02 0.28 0.25* 0.21

SF-36 Physical component scale

0.43* 0.47* 0.36 0.52* 0.51*

SF-36 Mental component scale

-0.34* -0.32* 0.49* 0.04 0.03

60

Floor and ceiling effects were not observed in both versions of the questionnaire, as only 1

subject (1%) scored 0 points, nobody scored 100 points, and 1 patient scored the maximum

of 60 points in the modified VISA-A score.

DiscUssioN

The aim of this study was to translate the original VISA-A questionnaire on the subjective

complaints of patients with Achilles tendinopathy into the Dutch language, to validate it, and

to assess its applicability to non-athletes.

The translation procedure did not create any problems, since the items are universal and

there is no large cultural difference between Dutch and Canadian patients.

Reliability of the translation was excellent, with a statistically not significant difference

between assessments. This outcome may be explained by the fact that, as the procedure

for the Dutch Oxford 12-item knee questionnaire taught us12, we introduced a question if

complaints had changed between assessments. 15/67 patients (22%) answered this ques-

tion with ‘yes’, and therefore they were excluded from reliability testing.

The smallest detectable change (SDT) in this study indicates that under stable condition,

the VISA-A score can vary up to 12 points. For clinical studies, this implies that clinical changes

can only be detected if they exceed the 12 points.

The study questionnaire showed good internal consistency (Crohnbach’s alpha 0.80), but

there indeed was a negative effect of the activity domain. Subanalysis without these ques-

tions showed an increase of Crohnbach’s alpha to 0.88. However, when measuring the effect

of a treatment in a mixed group of athletes and non-athletes, the effect of treatment could

be underestimated. For example, an athlete can score 0 points with question 7 and 8 before

treatment as complaints withhold him/her from being sports active. After treatment, the

athlete is complaint-free and scores 100 points. The non-athlete also scores 0 points for

questions 7 and 8 before treatment, and is also complaint-free after treatment. However,

he/she will never score higher than 60 points as question 7 and 8 will not be answered

differently between assessments. The effect of treatment, when using the VISA-A score to

measure outcome, is therefore underestimated in non-athletes.

When choosing the VISA-A questionnaire for a mixed population of athletes and non-

athletes, deleting questions 7 and 8 can be considered, since the psychometric properties of

the modified VISA- A were comparable with the original version.

Generally Pearson correlation coefficients were higher for physical than psychological

components. Convergent and divergent validity is confirmed as correlation coefficients were

higher for the physical domains of the questionnaires. However, for non-athletes correlation

with socio- emotional components was also higher. This could imply that physical restrictions

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in this subgroup with chronic Achilles tendinopathy have greater emotional and social conse-

quences than in athletes. Noticeable is the moderate correlation of VISA-A with VAS, which

is a validated subjective outcome measure frequently used for scientific means.

Low correlations can be explained by the fact that none of the questionnaires except for the

VISA-A were validated for Achilles tendinopathy. Initially it was intended to do so, but this

study aim was departed to not further enlarge patient burden as many of these question-

naires are extensive. Given the laborious inclusion of 104 patients in 3.5 years and 56%

response rate to both assessments this was well decided. This was also why responsiveness

was not tested.

coNcLUsioN

The VISA-A-NL questionnaire seems suitable for use in athletes. However, in a combined

population of atletes and non-athletes results will become incomparable as the highest pos-

sible score for non-athetes is 40 points lower than for non-athletes. Psychometric properties

of the VISA-A-NL, without questions 7 and 8, are satisfactory for both athletes and non-

athletes. It is therefore proposed that the modified VISA-A-NL questionnaire is considered in

a mixed population of patients with Achilles tendinopathy.

62

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Translation, validation, and norming of the

Dutch language version of the SF-36 Health

Survey in community and chronic disease

populations. J Clin Epidemiol 1998; 51(11):

1055-1068.




30(20-22): 1646-1650.

3. Beaton DE, Bombardier C, Guillemin F, Fer-

raz MB. Guidelines for the process of cross-

cultural adaptation of self-report measures.

Spine 2000; 25(24): 3186-3191.

4. Beckerman H, Roebroeck ME, Lankhorst

GJ, Becher JG, Bezemer PD, Verbeek AL.

Smallest real difference, a link between

reproducibility and responsiveness. Qual Life

Res 2001; 10(7): 571-578.

5. Brazier JE, Harper R, Jones NM et al. Validat-

ing the SF-36 health survey questionnaire:

new outcome measure for primary care.

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6. Dawson J, Carr A. Outcomes evaluation in

orthopaedics. J Bone Joint Surg Br 2001;

83(3): 313-315.

7. Dunbar MJ, Robertsson O, Ryd L, Lidgren L.

Translation and validation of the Oxford-12

item knee score for use in Sweden. Acta

Orthop Scand 2000; 71: 268-274.

8. Eechaute C, Vaes P, Duquet W, Van GB.

Test-retest reliability of sudden ankle inver-

sion measurements in subjects with healthy

ankle joints. J Athl Train 2007; 42(1): 60-65.

9. Fleiss JL. The design and analysis of clinical

experiments. 1986. New York, Wiley.

10. Guillemin F. Cross-cultural adaptation and

validation of health status measures. Scand J

Rheumatol 1995; 24(2): 61-63.

11. Guillemin F, Bombardier C, Beaton D. Cross-

cultural adaptation of health-related quality

of life measures: literature review and

proposed guidelines. J Clin Epidemiol 1993;

46(12): 1417-1432.

12. Haverkamp D, Breugem SJ, Sierevelt IN,

Blankevoort L, van Dijk CN. Translation and

validation of the Dutch version of the Oxford

12-item knee questionnaire for knee arthro-

plasty. Acta Orthop 2005; 76(3): 347-352.

13. Insall JN, Dorr LD, Scott RD, Scott WN.

Rationale of the Knee Society clinical rating

system. Clin Orthop Relat Res 1989; (248):

13-14.

14. Kitaoka HB, Alexander IJ, Adelaar RS, Nunley

JA, Myerson MS, Sanders M. Clinical rating

systems for the ankle-hindfoot, midfoot,

hallux, and lesser toes. Foot Ankle Int 1994;

15(7): 349-353.

15. Lohrer H, Nauck T. Cross-cultural adaptation

and validation of the VISA-A questionnaire

for German-speaking Achilles tendinopathy

patients. BMC Musculoskelet Disord 2009;

10(1): 134.

16. Maffulli N, Longo UG, Testa V, Oliva F,

Capasso G, Denaro V. Italian translation of

the VISA-A score for tendinopathy of the

main body of the Achilles tendon. Disabil

Rehabil 2008; 30(20-22): 1635-1639.

17. Mathias SD, Fifer SK, Patrick DL. Rapid

translation of quality of life measures for

international clinical trials: avoiding errors

in the minimalist approach. Qual Life Res

1994; 3(6): 403-412.

18. Price DD, McGrath PA, Rafii A, Buckingham

B. The validation of visual analogue scales

as ratio scale measures for chronic and

experimental pain. Pain 1983; 17(1): 45-56.





335-341.




Int 2001; 22(10): 788-794.

21. Silbernagel KG, Thomee R, Karlsson J.

Cross-cultural adaptation of the VISA-A

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questionnaire, an index of clinical severity

for patients with Achilles tendinopathy, with

reliability, validity and structure evaluations.

BMC Musculoskelet Disord 2005; 6: 12.

22. Streiner DL. Starting at the beginning: an

introduction to coefficient alpha and inter-

nal consistency. J Pers Assess 2003; 80(1):

99-103.

23. Sullivan LM, Dukes KA, Harris L, Dittus RS,

Greenfield S, Kaplan SH. A comparison of

various methods of collecting self-reported

health outcomes data among low-income

and minority patients. Med Care 1995; 33(4

Suppl): AS183-AS194.

24. Terwee CB, Bot SD, DE Boer MR et al. Qual-

ity criteria were proposed for measurement

properties of health status questionnaires. J

Clin Epidemiol 2007; 60(1): 34-42.

25. van Dijk CN, van Sterkenburg MN, Wieger-

inck JI, Karlsson J, Maffulli N. Terminology

for Achilles tendon related disorders. Knee


835-41.

26. Ware JE, Jr., Sherbourne CD. The MOS

36-item short-form health survey (SF-36). I.

Conceptual framework and item selection.

Med Care 1992; 30(6): 473-483.

64

Addendum- Dutch translation of VISA-A questionnaire

VISA-A-NL VRAGENLIJST

Geboortedatum: / / Datum:

Naam:

IN DEZE VRAGENLIJST STAAT HET BEGRIP ‘PIJN’ SPECIFIEK VOOR PIJN IN DE OMGEVING VAN UW ACHILLESPEES

1. Hoeveel minuten heeft u stijfheid in de omgeving van uw achillespees nadat u ’s ochtends bent op-gestaan?

100 min of langer

0 min PUNTEN

0 1 2 3 4 5 6 7 8 9 10

2. Heeft u, na het ‘op gang komen’ ’s ochtends, pijn bij het maximaal rekken van de achillespees op de rand van een verhoging (bijvoorbeeld traptrede)? (met de knie gestrekt)

Extreem hevige pijn

geen pijn

PUNTEN

0 1 2 3 4 5 6 7 8 9 10

3. Volgt er pijn in de eerste 2 uur na een 30 minuten durende wandeling op een vlakke ondergrond? (Als u door de pijn geen 30 minuten kúnt lopen op een vlakke ondergrond, vul da ‘0’ in bij deze vraag).

Extreem hevige pijn

geen pijn

PUNTEN

0 1 2 3 4 5 6 7 8 9 10

4. Heeft u pijn wanneer u normaal de trap af zou lopen?

Extreem hevige pijn

geen pijn

PUNTEN

0 1 2 3 4 5 6 7 8 9 10

5. Heeft u pijn tijdens of direct nadat u 10 keer (op één been) op uw tenen gestaan heeft op een vlakke ondergrond?

Extreem hevige pijn

geen pijn

PUNTEN

0 1 2 3 4 5 6 7 8 9 10

6. Hoe vaak kunt u hinkelen zonder pijn?

0 10 of meer

PUNTEN

0 1 2 3 4 5 6 7 8 9 10

7. Doet u op dit moment aan sport of een andere vorm van lichaamsbeweging?

0Helemaal niet

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4Aangepast trainingsschema/ trainingsniveau en aangepaste competitie

7Volledige training en volledige competitie, maar op lager niveau dan voor het ontstaan van de klachten

PUNTEN

10Competitie en training op hetzelfde of hoger niveau dan voor aanvang van de klachten

8. Van de volgende vraag dient u alleen A, B OF C te beantwoorden.

* U vult vraag A in indien: u GEEN pijn ervaart tijdens sportactiviteiten die de achillespees

belasten

* U vult vraag B in indien: u tijdens sportactiviteiten die de achillespees belasten pijn

ervaart waarbij u de sportactiviteit NIET hoeft te staken

* U vult vraag C in indien: u tijdens sportactiviteiten die de achillespees belasten een

zodanige pijn ervaart dat u uw activiteit MOET staken.

A. Indien u geen pijn heeft tijdens sportactiviteiten die de achillespees belasten, hoe lang bent u dan in staat te sporten/ trainen?

NIET 1-10 min

11-20 min

21-30 min

>30 min

PUNTEN

0 7 14 21 30

OF B. Indien u enige pijn heeft tijdens sportactiviteiten die de achillespees belasten maar waarbij u de activiteit wel af kunt maken, hoe lang bent u dan in staat te sporten/trainen?

NIET 1-10 min

11-20 min

21-30 min

>30 min

PUNTEN

0 4 10 14 20

OF C. Indien u tijdens sportactiviteiten die de achillespees belasten een zodanige pijn heeft dat u de activiteit moet stoppen, hoe lang bent u dan toch in staat geweest te sporten/trainen?

NIET 1-10 min

11-20 min

21-30 min

>30 min

PUNTEN

0 2 5 7 10

TOTALE SCORE ( /100)%

PArt iii miDPortioN AchiLLes

teNDiNoPAthY: cAUse of PAiN AND treAtmeNt moDALities

Chapter 4

Less promising results with sclerosing Ethoxysclerol injections for

midportion Achilles tendinopathy

A retrospective study

MN van Sterkenburg

MC de Jonge

IN Sierevelt

CN van Dijk

Am J Sports Med 2010; 38: 2226-2232

70

ABstrAct

BackgroundIn patients with complaints of chronic midportion Achilles tendinopathy, neovascularisation

around the Achilles tendon and structural changes in the area were observed, but not in pain

free normal tendons. Local injections of the sclerosing substance Polidocanol (Ethoxysclerol)

have shown to yield good clinical results in patients with chronic Achilles tendinopathy. After

training by the inventors of the technique, sclerosing Ethoxysclerol injections were applied on

a group of patients in our center.

HypothesisWe hypothesized that sclerosing Ethoxysclerol injections did not yield good results in the

majority of patients.

Study designRetrospective cohort study with 2.7-5.1 year follow-up.

MethodsIn 113 patients (140 tendons) with midportion Achilles tendinopathy, 62 patients (70 tendons)

showing neovascularisation on colour Doppler ultrasound (US) were identified. 53 Achilles

tendons (48 patients) were treated with sclerosing Ethoxysclerol injections, with intervals of

6 weeks and a maximum of 5 sessions. Treatment was completed when neovascularisation

or pain had disappeared, or when there was no positive treatment effect after 3-4 sessions.

ResultsFourty-eight patients (20 females and 28 males) with a median age of 45 (33-68) years, were

treated. Median symptom duration was 23 months (range 3 to 300). Fifty-three tendons

were treated with a median of 3 sessions of Ethoxysclerol injections. Six weeks after the

last injection, 35% had no complaints, 9% minimal, 42% had the same and 14% had

more complaints. Pain correlated positively with neovessels on US (p<0.01). At 2.7-5.1 year

follow-up, 53% had received additional (surgical/ conservative) treatment, and 3 of these

patients (7.5%) still had complaints of midportion Achilles tendinopathy. In 6 complaints

after six weeks had resolved spontaneously.

ConclusionOur study did not confirm the high beneficial value of sclerosing neovascularisation in

patients with midportion Achilles tendinopathy.

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Clinical RelevanceIn recent years good results on the injection of sclerosing Ethoxysclerol have been reported,

which we were not able to reproduce. Despite the retrospective design of our study, we

consider it important to stress that injection of Ethoxysclerol may not be as promising as was

thought.

72

iNtroDUctioN

Chronic midportion Achilles tendinopathy is a common painful condition that is generally dif-

ficult to treat. It is defined as a painful thickening of the tendon typically 2-7 cm proximal to

its insertion in the calcaneus, without an inflammatory cellular response inside the tendon2.

Often it is accompanied by paratendinopathy. Complaints consist of long-term pain, tender-

ness and stiffness. The most apparent finding from clinical examination is a painful nodule

on palpation of the Achilles tendon. On ultrasound (US) or Magnetic Resonance Imaging

(MRI) examination thickening of the tendon and structural abnormalities in the painful area

are seen.

Currently, a wide range of conservative treatments is available for midportion Achilles

tendinopathy such as cast immobilisation, night splint, heel-raise, wait-and-see policy,

friction therapy, shock-wave treatment, and eccentric training of the muscle-tendon com-

plex6,32,34,38,45.

Studies on eccentric training have generally showed good outcomes in the majority of

patients6,14,26,31,39,42. Other studies have not been able to replicate these results12,38. When

conservative measures fail surgical treatment is indicated. To reduce the necessity of surgical

interference, new conservative measures have been developed worldwide. In 2002, a new

type of injection therapy was introduced30.

Using colour Doppler ultrasound, neovascularisation on the ventral side of the Achilles

tendon was demonstrated in symptomatic patients21. Normal tendons lack these changes.

It was hypothesized that neovessels and accompanying nerves were responsible for the

pain in Achilles tendinopathy. Local injections of these areas with neovascularisation with

Polidocanol (Ethoxysclerol) gave good clinical results in a double blind randomised controlled

trial on patients with chronic Achilles tendinopathy5,30. At 2-year follow-up, they showed

remaining good clinical results25.

One of our radiologists specialized in musculoskeletal radiology, was trained by the inven-

tors of the procedure to perform it according to the method as originally described30. From

August 2004 until February 2007 48 patients were treated with Ethoxysclerol injections for

chronic midportion Achilles tendinopathy. The purpose of this study was to analyze our

results of this new intervention.

methoDs

Between August 2004 and February 2007, a total of 113 consecutive patients with 140

symptomatic Achilles tendons underwent colour Doppler ultrasonography investigation

(US). Patients with midportion Achilles tendinopathy and neovascularisation were offered

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treatment with Ethoxysclerol. Sixty-two patients had 70 symptomatic tendons showing

neovascularisation (50%). In 50% of tendons with Achilles tendinopathy no neovessels were

found. Fourteen patients were excluded from treatment because they refused sclerosing

therapy (Figure 1). Results of these injections were retrospectively analyzed.

Ultrasonography and colour Doppler examination (US)All tendons were examined with high-resolution greyscale ultrasound and with colour

Doppler. A linear 17 MHz transducer was used. Achilles tendons showing midportion ten-

dinopathy with neovascularisation, and accompanying clinical data concerning age, gender,

symptom duration, presence and amount of neovascularisation, frequency of injections, and

complaints after treatment were extracted.

Injection of EthoxysclerolEthoxysclerol has a selective effect in the vascular intimae, causing thrombosis of the vessel,

even if the injection is performed extravasally, which is important when very small vessels are

targeted16. It also has a local anaesthetic effect.

Only patients, who already underwent six months of conservative treatment including

physical therapy involving eccentric training for their current complaints, were offered this

treatment.

If patients had at least a minimal amount of injectable neovascularisation (Figure 1) around

their Achilles tendon on US, they were injected with Ethoxysclerol. Patients were in prone

position, and the skin was washed with chlorohexidin 0.5% in 70% alcohol. For injection, a

23 gauge needle connected to a 3 ml syringe was used.

Figure 1. Number of tendons with neovascularisation and inclusion

74

The injections at the target vessels were performed under US guidance, from the medial

side of the Achilles tendon to minimise the risk of sural nerve injury. Ethoxysclerol (2-4 ml)

was injected until neovessels were no longer visible on US. After injection, a compressive

bandage was applied. Patients were instructed to take the bandage off 24 hours after treat-

ment, and free activity such as walking, bicycling, and light strength training were allowed

the first 2 weeks. After these 2 weeks, free tendon loading activity was allowed.

Six weeks after treatment patients were assessed again by US, and if they still had com-

plaints and neovascularisation injection with Ethoxysclerol was repeated, with a maximum

of 5 treatments. Treatment was completed when no neovascularisation was present on US,

when pain had disappeared, or when there was no positive treatment effect after 3 to 4

sessions. The same radiologist performed all US examinations and treatments.

Follow-upThe primary outcomes were defined as persistent pain and the absence or presence of neo-

vascularisation. Patients were retrospectively questioned about the amount of pain six weeks

after treatment as described on a 4- point scale as being no, minimal, same, or more. The

amount of neovessels present after sclerosing therapy was described likewise as being no,

minimal, same, or more by the radiologist performing the procedure. Information on weight,

sports activity, employment, comorbidity and medication was taken.

Subjective outcome at midterm follow-up (2.7-5.1 years; mean 3.9 years) was assessed

using the same 4- point scale (no, minimal, same, or more), Visual Analogue Scales (VAS)

for pain and function, and the Victorian Institute of Sports Assessment- Achilles (VISA-A)

questionnaire. This questionnaire was created in 2001 to assess clinical severity for patients

with Achilles tendinopathy. It is a self- administered questionnaire evaluating symptoms and

their effect on physical activity36. Information was gathered on current sporting activity and

interventions in the past years after sclerosing injections.

Statistical analysis All obtained data were entered in a database and statistical analysis was performed using

SPSS 15.0, (SPSS Inc., Chicago, IL, USA). Due to skewed distributions, continuous data (e.g.

age, VAS, VISA-A) were described as medians and ranges and analysed non-parametrically.

Categorical and dichotomous data (e.g. pain after treatment, complaints, amount of neovas-

cularisation) were presented as frequencies and accompanying proportions. Wilcoxon Rank

Sum test was performed to assess the change in sport activities/duration before and during

complaints of the Achilles tendon, and to investigate change in pain level at six weeks and

mid-term follow-up.

Spearman’s correlation coefficient was calculated to determine the association between

pain level and amount of neovessels at six weeks follow-up, and pain level and several demo-

graphic factors (symptom duration, age and BMI) at mid-term follow-up.

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To assess whether gender significantly influenced complaints, we dichotomised com-

plaints to none/minimal and same/more. Chi-square tests were performed and Odds- ratios

(with 95%CI) were calculated. Mann Whitney U-tests were performed to assess difference in

age between nine/minimal and same/more complaints and to assess a learning curve of the

injection procedure. Therefore, we compared the dichotomised complaints six weeks after

injection from the first and the last 15 patients.

Reported P values were 2-sided and were considered significant if p<.05.

resULts

Patient populationDemographics are summarized in table 1.

Table 1. Demographics

Patients with Achilles tendinopathy

Patients with neovascularisation

Patients treated with sclerosing injections

Age (years)median (min-max) 46 (14-81) 47 (14-79) 45 (33-68)

Gender (m/f) 60 (53%)/53 (47%) 35 (56%)/27 (44%) 28 (70%)/20 (30%)

Side (l/r) 80 (57%)/60 (43%) 38 (54%)/32 (46%) 31 (58%)/22 (42%)

Forty-eight patients (53 tendons) were treated. Eleven patients (12 tendons) were lost to

follow-up and one patient deceased. Thirty six patients (75%) with 40 treated tendons, 19

male and 17 female, with a median age of 50 (range; 38-72) and BMI of 25.9 (range; 21-39),

returned the questionnaires for follow-up.

Median symptom duration before sclerosing was 23 months (range; 3-300). Five patients

had comorbidity: cardiovascular symptoms (n=2), CRPS (n=1), fibromyalgia (n=1) and lipo-

edema of the legs (n=1). Nine patients used prescription drugs; of these 2 used inhalation

glucocorticosteriods and the others used different medication for pain and cardiovascular

disease.

Most subjects (58%) had fulltime employment in a physical or office setting. Prior to

complaints, 30 out of the 36 patients (83%) were sports active. The most common activities

were running (39%), tennis (22%) and soccer (14%). Sport level was recreational for 24

patients (67%), competitive for 11 patients (31%), and professional for 1 patient (2%).

Median hours of sports activity a week was 4 (range; 0-30).

During complaints of midportion Achilles tendinopathy, 7 patients were unable to con-

tinue playing any sports and 1 voluntarily quit. Median number of hours a week playing

sports diminished to 1 (range; 0-30) (p=0,00). Seven patients were still able to continue their

activities on a competitive level.

The type of conservative treatment prior to sclerosing injections is shown in table 2.

76

Fifty-three symptomatic tendons were treated with a median of 3 sessions (range; 1-7) of

Ethoxysclerol injections (Table 3). Fifty-six percent of patients rated the injections as unpleas-

ant.

Short term results (6 weeks after the last injection)All patients, except one, returned to work within 2 days after injection with Ethoxysclerol

(median 0.0, range; 1-7 days). Of the 30 patients who were sports active before complaints,

18 patients (60%) resumed sporting activities, 12 (67%) at the same level, 5 (28%) on a

lower level and 1 (5%) on a higher level. Median time to sports resumption was 2 weeks

(0-104).

At 6 weeks follow-up 40 patients (45 tendons) showed up for US. Decrease of neovascu-

larisation was present in 21 tendons (47%) (Table 4) and patients experienced pain relief in

19 treated tendons (44%): 15 (35%) caused no pain and 4 (9%) still produced minimal pain;

42% still experienced the same pain and 14% even had more pain.

Spearman’s correlation coefficient showed a moderate correlation between the amount

of neovessels observed on Doppler ultrasound and the pain level experienced by the patient

(r=0.48, p=0.001).

Table 2. Most common types of conservative measures prior to injection with Ethoxysclerol

Conservative measures prior to sclerosing injections (n=46)

Physical therapy (eccentric training, friction, stretching) 40 (87%)

Cast immobilization 12 (26%)

Inlays 7 (15%)

Cortisone injection 13 (28%)

Rest 26 (57%)

NSAIDs 3 (7%)

Table 3. Number of injections per tendon

Number of injections per tendon Frequency (%)

1 14 (26%)

2 11 (21%)

3 15 (28%)

4 6 (11%)

5 6 (11%)

6 0 (0%)

7 1 (1.9%)

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77Six weeks after treatment, significantly more male patients (58%) had no or minimal com-

plaints than female patients (26%) (p=0.04). The odds ratio for females compared to males

having the same or more complaints after treatment was 3.8 (95% CI 1.1-13.8), which

means they had a 3.8 times higher chance of an unsatisfying outcome than males. Age did

not significantly affect outcome (p=0.09). The median age of patients with no or minimal

complaints after treatment was 43.5 (range; 33-68) years, and for patients with same or

more complaints 49.0 (range; 35-60).

We could not identify a learning curve for performing the treatment. The outcome in

the first 15 patients demonstrated that 56% to experienced no/minimal pain while 44% of

patients demonstrated the same or more pain at follow-up. Results of treatment in the last

15 patients showed that 43% of these patients had none/ minimal pain whilst 57% had the

same or more pain (p= 0.46).

Results at mid-term follow-up: 3.9 (range; 2.7-5.1) yearsMedian VISA-A score was 82 points (range; 20-100), median VAS for pain was 0 mm (range;

0-82) and for function 99 mm (range; 14-100).

Of the 40 tendons (of the 36 patients who had returned the questionnaire), 21 (53%) had

additional treatment in the years following sclerosing injections. Fifteen tendons (71%) were

treated operatively (open surgical debridement or Achilles tendoscopy), sometimes in com-

bination with conservative treatment (2 tendons). The other 6 tendons (29%) were treated

with different conservative measures. Of patients with 21 additionally treated tendons, 18

(86%) had the same or more complaints six weeks after injection and 3 (14%) had minimal

complaints. Of patients with 19 tendons who did not report seeking additional treatment, 6

(32%) had same/more complaints and 13 (69%) had no complaints after six weeks follow-

up. The 6 with same/ more complaints at six weeks had no complaints at mid-term follow-up

without additional treatment.

The level of pain had significantly decreased at mid-term follow-up compared to six-week

follow-up (p<0.01) (Diagram 1).

Of the 40 tendons at mid- term follow-up, 3 (7.5%) still showed the same or more com-

plaints, even after additional surgical or conservative treatment.

Table 4. Information on the quantity of neovascularisation present 6 weeks after the last injection was present in 45 treated tendons. In 8 this outcome was not described

Neovascularisation 6 weeks after treatment Tendons (n= 45)

No 5 (11%)

Less 16 (36%)

Same 20 (44%)

More 4 (9%)

78

No significant correlations were observed between complaints at midterm follow-up and

symptom duration, age, and BMI.

DiscUssioN

We could not demonstrate a beneficial effect of Ethoxysclerol injections in patients with mid-

portion Achilles tendinopathy as opposed to earlier published results of this treatment5,25.

Only 44% of tendons were painless or minimally painful at six weeks after treatment with

Ethoxysclerol.

At 2.7-5.1 year follow-up 53% of all treated tendons had undergone additional treat-

ment (nonoperative or surgical).

The treatment of chronic tendinopathy of the Achilles tendon with Ethoxysclerol as introduced

by Alfredson and Ohberg in 2002 appeared to be a promising method of treatment30. It was

hypothesized that neovessels and accompanying nerves were responsible for the pain in mid-

portion Achilles tendinopathy. After a pilot study in 2002 in which they treated 10 patients,

8 of whom had favourable outcome, they further developed their technique resulting in a

publication in 2005 in which the outcome of a double-blind randomised trial was published.

Patients were injected with either Ethoxysclerol or lidocain combined with adrenalin5. The

study showed that 10 out of 10 patients reported satisfaction with the result of the treatment

with a significant improvement on VAS. Nine out of 10 patients in the control group reported

Diagram 1. Outcome of pain at 6 weeks and 2.7-5.1 years after sclerosing therapy

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satisfaction, but the difference in VAS before and after the treatment in the Ethoxysclerol

group was significantly larger. Also, patients in the sclerosing group showed no remaining

neovascularisation on colour Doppler5. Extending their proposed pathophysiological prin-

ciples of midportion Achilles tendinopathy and the role of neovessels in patellar tendinopathy

they applied the same treatment regime of injecting a sclerosing agent into these patients

in 2005, again with promising results4. In 2006, the group published the results of the first

2-year follow-up which showed remaining good clinical results and a lasting decrease in vol-

ume of the Achilles tendon. The favourable outcome in patients treated with this technique

has also been published by Clementson and co-workers in 2008 in a retrospective study of

25 patients9. The technique has currently been introduced by Alfredson and co-workers for

the treatment of painful tennis elbow and shoulder impingement syndromes1,3,47. All this

suggests a beneficial value of Ethoxysclerol in midportion tendinopathy.

A possible reason for our less favourable outcome is the retrospective design of our study.

We did not use neovascularisation scores or valid subjective outcome measures at six

weeks follow-up. Treatment in our clinic was initially not set up as a clinical trail but we just

implemented it as a new conservative measure for midportion Achilles tendinopathy. The

reason for this was the high percentage of good and excellent results in various publications

by the group of Alfredson indicating injection therapy to be a valuable treatment strategy.

As opposed to a good outcome, patients reported low satisfaction all along the way. We

considered this important to report, irrespective of the retrospective design.

Our success-rate from the injection of Ethoxysclerol is close to placebo-controlled studies

on conservative measures such as corticosteroid injections and external triglyceryltrinitrate

application, as well as the administration of placebo. These treatments also yield positive

results in 33-49% of patients10,32, well below the success percentage of eccentric training

and various surgical approaches. Eccentric loading should be the very first treatment method

for patients with midportion Achilles tendinopathy, since this treatment modality has been

tested in a proper manner and yields good results6,37-39. However, the training programme

is extensive, painful and requires strong perseverance. Eighty- seven percent of our patients

reported to be subjected to an eccentric training program guided by a physiotherapist before

being offered Ethoxysclerol injections, without a beneficial outcome. This may be a subgroup

not responding to eccentric training, or it may be due to inadequate instructions or insuf-

ficient compliance.

Injection with Ethoxysclerol is a conservative treatment method and positive outcome in 44%

of patients might be sufficient to implement this therapy as primary or secondary treatment

option for some patients with symptomatic midportion Achilles tendinopathy. On the other

hand, with an average of 2.7 injections with intervals of six to eight weeks it is an unpleasant

80

and time-consuming conservative treatment. This might particularly be problematic in active

patients and professional athletes demanding a quicker solution to return to sports.

The origin of pain in midportion Achilles tendinopathy, its natural history and the mecha-

nism by which a wide range of treatments generates relief is largely unknown. Sclerosing

treatment is based on the hypothesis that neovessels at the ventral side of the Achilles

tendon accompanied by nerves are the cause of pain. However, of 140 Achilles tendons

with clinically and ultrasonographically demonstrated Achilles tendinopathy, only 70 tendons

showed neovascularisation (50%). De Vos-, Peers-, Reiter- and Zanetti and co-workers found

equal proportions of neovascularisation in 50-88% of symptomatic tendons11,33,35,46.

The focus of treating Achilles tendinopathy is on relieving pain. Most often the intraten-

dinous changes are addressed. However, it is questionable if degeneration of the tendon

itself is the main cause of pain, since intratendinous changes are found in up to 34% of

people without complaints13,15,18,19. Very recently a long-term follow-up study was published

revealing persistent structural abnormalities and thickening of the tendon 13 years after

intra-tendinous surgery for Achilles tendinopathy, whereas all patients were satisfied with

the results and went back to Achilles tendon loading activities without restrictions7. Mid-

portion Achilles tendinopathy and paratendinopathy often co-exist43. Adhesions between

the tendon, peritendineum and crural fascia in the chronic phase are formed, prohibiting a

normal gliding movement of the tendon. The healthy tendon proper is normally aneuronal8,

but chronic painful tendons have been shown to exhibit new ingrowth of sensory nerve

fibers in the tendon proper24,41. We theorize that ‘denervation’ of the tendon is sufficient

to relieve symptoms. With Ethoxysclerol, by addressing neovessels, nerves are probably also

attacked. Injection may not suffice because of low volume and effectiveness of the substance

on nerves, and adhesions are too solid to be adequately released.

In agreement with this theory, surgical release of these adhesions though an open

approach17,20,22,23,29,40 or via endoscopically assisted techniques27,28,43,44, leaving the ten-

don proper untouched has demonstrated to be effective and provides quick rehabilitation.

However, these series are small and follow-up is of short duration. Fundamental research and

larger comparative series on surgical measures need to be done with proper study design

and at least one year follow-up to verify the cause of complaints before optimal treatment

can be developed.

coNcLUsioN

Our study did not confirm a beneficial value of sclerosing Ethoxysclerol injections in patients

with midportion Achilles tendinopathy. On the basis of our results, we decided to discontinue

the implementation of this treatment in our clinic.

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22. Leach RE, Schepsis AA, Takai H. Long-term

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23. Lehto MU, Jarvinen M, Suominen P. Chronic

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GA. Topical glyceryl trinitrate treatment of

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34. Perlick L, Schiffmann R, Kraft CN, Wallny T,

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koff D, Bucek RA. [Extended field-of-view

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index of the clinical severity of Achilles tendi-

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loading versus eccentric loading plus shock-

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Am J Sports Med 2009; 37: 463-470.

38. Rompe JD, Nafe B, Furia JP, Maffulli N.

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a wait-and-see policy for tendinopathy of the

main body of tendo Achillis: a randomized

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controlled trial. Am J Sports Med 2007; 35:

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Soderberg B. Clinical improvement after 6




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ment of Achilles tendinitis. Am J Sports Med

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F, Straub RH. Achilles tendinosis is associated

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polidocanol injections in chronic painful ten-

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14: 1218-1224.

Chapter 5

Endoscopy of tendons around the ankle

Officially translated to German

Tendoskopie am Sprunggelenk und Fuß

MN van Sterkenburg

PAJ de Leeuw

CN van Dijk

Artroskopie 2009; 22: 132-140

86

ABstrAct

Ankle arthroscopy is increasingly used as a technique for dealing with a wide range of ankle

pathologies. In contrast, extra-articular problems of the ankle still most often demand open

surgery. In the recent years, endoscopic procedures for treating various tendon pathologies

have been developed. Like arthroscopic surgery, tendoscopy offers the advantages related

to any minimally invasive procedure such as fewer wound infections, less blood loss, smaller

wounds and less morbidity. This article defines the major indications in which tendoscopy is

appropriate and presents current techniques for treatment.

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iNtroDUctioN

In contrast to arthroscopy, which has become the preferred technique to treat intra-articular

ankle pathology, extra-articular problems of the ankle have traditionally demanded open sur-

gery. Open ankle surgery has been associated with complications such as injury to the sural

nerve or superficial peroneal nerve, infection, scarring, and stiffness of the ankle joint1,12,29.

The percentage of complications reported with open surgery for posterior ankle impinge-

ment (removal of os trigonum, scar tissue, hypertrophic posterior talar process, or ossicles)

varies between 15 and 24%1,12,29,50. The incidence of these complications has stimulated

the development of extra- articular endoscopic techniques. Endoscopic surgery offers the

advantages related to any minimally invasive procedure, such as fewer wound infections, less

blood loss, smaller wounds and less morbidity. Aftertreatment is functional, and surgery is

performed on an outpatient basis46.

Tendoscopy can be performed for the treatment and diagnosis of various pathologic

conditions of the peroneal tendons, the posterior tibial tendon, and the Achilles tendon. In

this manuscript, we describe these procedures and their indications.

1. teNDoscoPY of the PeroNeAL teNDoNs

IntroductionPathology of the peroneal tendons is most often seen with, and secondary to chronic lat-

eral ankle instability. These disorders frequently cause chronic ankle pain in runners and

ballet dancers6. Post-traumatic lateral ankle pain is seen frequently, but peroneal tendon

pathology is not always recognized as a cause of these symptoms. In a study by Dombek

and co-workers, only 60% of peroneal tendon disorders were accurately diagnosed at the

first clinical evaluation11. Because the peroneal tendons act as lateral ankle stabilizers, in

chronic instability of the ankle more strain is put on these tendons, resulting in hypertrophic

tendinopathy, tenosynovitis, and ultimately in tendon tears39.

Anatomically, the peroneus brevis tendon is situated dorsomedially to the peroneus longus

tendon from its proximal aspect up to the fibular tip, where it is relatively flat. Just distally

to this tip, the peroneus brevis tendon becomes rounder, and crosses the round peroneus

longus tendon. The distal posterolateral part of the fibula forms a sliding channel for the two

peroneal tendons. This malleolar groove is formed by a periosteal cushion of fibrocartilage

that covers the bony groove. The tendons are held into position by the superior peroneal

retinaculum39,47,49.

Pathology of the peroneal tendons consists of tenosynovitis, tendon dislocation or sublux-

ation, and (subtotal) rupture or snapping of one or both of the peroneal tendons. It accounts

for the majority of symptoms at the posterolateral aspect of the ankle37, 40. Other causes

of posterolateral ankle pain are rheumatoid synovitis, bony spurs, calcifications or ossicles,

88

pathology to the posterior talofibular ligament (PTFL), or disorders of the posterior compart-

ment of the subtalar joint. Posterior ankle impingement can present as posterolateral ankle

pain. On clinical examination, there is recognizable tenderness over the tendons on palpa-

tion. Swelling, tendon dislocation and signs of tenosynovitis can be found.

The diagnosis of peroneal tendon pathology can be difficult in a patient with lateral

ankle pain. A detailed history should include the presence of associated conditions such as

rheumatoid arthritis, psoriasis, hyperparathyroidism, diabetic neuropathy, calcaneal fracture,

fluoroquinolone use, and local steroid injections. These can all increase the prevalence of

peroneal tendon dysfunction13. A diagnostic differentiation must be made with fatigue

fractures or fractures of the fibula, posterior impingement of the ankle, and lesions of the

lateral ligament complex.

Additional investigations such as MRI and ultrasonography may be helpful in confirming

the diagnosis in (partial) tears of the tendon of peroneus brevis or longus54. Post-traumatic

or post-surgical adhesions and irregularities of the posterior aspect of the fibula (peroneal

groove) can also be responsible for symptoms in this region.

The primary indication of treating pathology of the peroneal tendons is pain. Conserva-

tive management should be attempted first. This includes activity modification, footwear

changes, temporary immobilization, and corticosteroid injections. Also, lateral heel wedges

can take the strain off the peroneal tendons which may allow healing. Failure of these

conservative measures may be an indication for surgery. We therefore developed a safe and

reliable endoscopic technique which we describe in detail here39,47.

Surgical techniqueThe patient is placed in the lateral decubitus position, with the operative side up. Before

anaesthesia is administered, the patient is asked to actively evert the affected foot. In this

way, the tendon can be palpated, and the location of the portals is drawn onto the skin. The

surgery can be performed under local, regional, epidural or general anaesthesia. A support is

placed under the affected leg making it possible to move the ankle freely. After exsanguina-

tion a tourniquet is inflated around the thigh of the affected leg.

A distal portal is made first, 2-2.5 cm distal to the posterior edge of the lateral mal-

leolus. An incision is made through the skin, and the tendon sheath is penetrated with an

arthroscopic shaft with a blunt trocar. After this, a 2.7 mm 30° arthroscope is introduced.

The inspection starts approximately 6 cm proximal from the posterior tip of the fibula, where

a thin membrane splints the tendon compartment into two separate tendon chambers. More

distally, the tendons lie in one compartment. A second portal is made 2-2.5 cm proximal to

the posterior edge of the lateral malleolus under direct vision by placing a spinal needle,

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producing a portal directly over the tendons (Figure 1). Through the distal portal, a complete

overview of both tendons can be obtained.

By rotating the arthroscope over and in between both tendons, the whole compartment

can be inspected. When a total synovectomy of the tendon sheath is to be performed, it is

advisable to produce a third portal more distal or more proximal than the portals described

previously.

When a rupture of one of the tendons is seen (Figure 2), endoscopic synovectomy is

performed, and the rupture is repaired through a mini-open approach.

In patients with recurrent dislocation of the peroneal tendon, endoscopic fibular groove

deepening can be performed through this approach. This is a time consuming proce-

dure, because of the limited working area. Groove deepening is performed from within the

Figure 1. Peroneal tendoscopy of the right ankle: (A) marking the anatomy of the peroneal tendons. (B) Arthroscopic view at introduction of the arthroscope looking from distal to proximal. An arrow indicates a thin membrane separating the two tendons proximally. (C) Placement of spinal needle under direct vi-sion for preparation of the second portal. (D) Endoscopic view of needle inside the tendon sheath. (PB= peroneus brevis, PL= peroneus longus)

90

tendon sheath with the risk of iatrogenic damage to the tendons. We therefore prefer an

approach by the 2 hindfoot portal technique47,50.

At the end of the procedure, the portals are sutured to prevent sinus formation, and a

compressive dressing is applied. Full weight bearing is allowed as tolerated and active range

of motion exercises are advised starting immediately post surgery.

ResultsWe reported the results of peroneal tendoscopy in 23 patients operated on between 1995

and 2000, with a minimum follow up of 2 years47. Eleven patients were diagnosed with

a longitudinal rupture of the peroneus brevis tendon; 8 of these presented with pain and

swelling over the posterior aspect of the lateral malleolus and 3 presented with a snapping

sensation at the level of the lateral malleolus.

Ten patients had persisting symptoms after surgery for a fracture of the fibula, lateral

ankle ligament reconstruction, or after operative repair of recurrent tendon dislocation.

Surgery consisted of endoscopic tenosynovectomy, adhesiolysis, removal of an exostosis,

and suturing a longitudinal rupture via a mini-open procedure. The two remaining patients

underwent endoscopic groove deepening of the fibular groove for complaints of recurrent

tendon dislocation.

No complications occurred, and complaints disappeared after surgery. Since then, we

performed another 28 procedures mainly for adhesiolysis, and diagnosis and management

of longitudinal ruptures. For recurrent peroneal tendon dislocation we treated another 12

patients by means of endoscopic groove deepening with good results at one year follow-up.

Figure 2. Peroneal tendoscopy in a 39-year-old male patient with a longitudinal tear of the right pero-neus brevis tendon. The arthroscope is introduced through the distal portal looking into a proximal direc-tion. Hypervascularisation (HV) of the peroneus brevis tendon as an expression of chronic irritation. (PB= peroneus brevis tendon, PL= peroneus longus tendon. The arrow indicates the tear.)

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The technique uses the 2 traditional hindfoot portals and one additional superoposterolateral

working portal50,10.

Lui and co-workers21 described an endoscopic technique to reconstruct the superior

peroneal retinaculum keeping the peroneal tendons in place when intact. In addition to

the two portals described earlier, retinacular openings are made slightly larger than the skin

openings of the portals. The lateral surface of the lateral malleolus where the retinaculum is

stripped off is roughened with an arthroscopic burr or curette. Three holes are drilled through

the portals with an interval of 1 cm, and three suture anchors are inserted into the fibular

ridge. A needle is inserted through the portal and the retinaculum pierced in an “inside-out”

manner. The sutures are pulled out and then retrieved at the surface of the retinaculum

through the skin wounds. When the sutures are tightened the retinaculum can be pushed

onto the fibular ridge. The authors describe 2 cases with good outcome, and a possible

great advantage could be that patients with endoscopic reconstruction seem to have less

subjective tightness as compared to those undergoing open procedures.

2. teNDoscoPY of the Posterior tiBiAL teNDoN

IntroductionIn the absence of intra-articular ankle pathology, posteromedial ankle pain is most often

caused by disorders of the posterior tibial tendon.

Inactivity of the posterior tibial tendon gives midtarsal instability and is the commonest

cause of adult onset flatfoot deformity. The relative strength of this tendon is more than

twice that of its primary antagonist, the peroneus brevis tendon. Without the activity of the

posterior tibial tendon, there is no stability at the midtarsal joint, and the forward propulsive

force of the gastrocnemius/soleus complex acts at the midfoot instead of at the midtarsal

heads. Total dysfunction eventually leads to a flatfoot deformity.

These disorders can be divided in two groups: the younger group of patients with dysfunc-

tion of the tendon, caused by some form of systemic inflammatory disease (e.g. rheumatoid

arthritis); and an older group of patients whose tendon dysfunction is mostly caused by

chronic overuse32.

Following trauma, surgery, and fractures, adhesions and irregularity of the posterior aspect

of the tibia can be responsible for symptoms in this region. Also, the vincula can become

symptomatic in these circumstances7,48. The vincula connect the posterior tibial tendon to its

tendon sheath49. Damage to the vincula can cause thickening, shortening and scarring of the

distal free edge. In these patients, a painful local thickening can be palpated posterior and

just proximal of the tip of the medial malleolus.

Mostly a dysfunctioning posterior tibial tendon evolves in a painful tenosynovitis. Tenosy-

novitis is also a common extra-articular manifestation of rheumatoid arthritis, where hindfoot

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problems are a significant cause of disability. Tenosynovitis in rheumatoid patients eventually

leads to a ruptured tendon30.

Although the precise aetiology is unknown, the condition is classified on the basis of clinical

and radiographic findings. In the early stage of dysfunction, patients complain of persisting

ankle pain medially along the course of the tendon, in addition to fatigue and aching on the

plantar medial aspect of the ankle. When a tenosynovitis is present, swelling is common. On

clinical examination, valgus angulation of the hindfoot is frequently seen, with accompanying

abduction of the forefoot, the “too-many-toes” sign45. This sign is positive when inspecting

the patient’s foot from behind: in case of significant forefoot abduction, 3 or more toes are

visible lateral to the calcaneus, where normally only 1 or 2 toes are seen.

Intra-articular lesions such as a posteromedial impingement syndrome, subtalar pathology,

calcifications in the dorsal capsule of the ankle joint, loose bodies or osteochondral defects

should be excluded. Entrapment of the posterior tibial nerve in the tarsal canal is commonly

known as a tarsal tunnel syndrome. Clinical examination is normally sufficient to adequately

differentiate these disorders from an isolated posterior tibia tendon disorder.

For additional investigation, magnetic resonance imaging (MRI) is the best method to

assess a tendon rupture18. Also, ultrasound imaging is known as a cost-effective and accu-

rate to evaluate disorders of the tendon31.

Initially, conservative management is indicated, with rest, combined with nonsteroidal anti-

inflammatory drugs (NSAIDS), and immobilization using a plaster cast or tape. There is no

consensus whether to use corticosteroid injections; some cases of tendon rupture following

corticosteroid injections have recently been described36.

After failure of 3-6 months of conservative management, surgery can be indicated22.

This can be performed open or endoscopically. An open synovectomy is performed by sharp

dissection of the inflamed synovium, while preserving blood supply to the tendon. Post-

operative management consists of plaster cast immobilization for 3 weeks with the possible

disadvantage of new formation of adhesions, followed by wearing a functional brace with

controlled ankle movement for another 3 weeks, and physical therapy5.

Endoscopic synovectomy is our surgical modality of choice when access allows radical

removal of inflamed synovium35. Several studies have been described previously in which

endoscopic synovectomy was successfully performed, offering the advantages that are

related to minimally invasive surgery47,48,49.

Surgical techniqueThe procedure can be performed on an outpatient basis under local, regional or general

anaesthesia. Patients are placed in the supine position. A tourniquet is placed around the

upper leg. Before anaesthesia, the patient is asked to actively invert the foot, so that the

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posterior tibial tendon can be palpated and the portals can be marked. Access to the tendon

can be obtained anywhere along the course of it.

We prefer to make the two main portals directly over the tendon 2-3 cm distal and 2-3

cm proximal to the posterior edge of the medial malleolus. The distal portal is made first: the

incision is made through the skin, and the tendon sheath is penetrated by the arthroscopic

shaft with a blunt trocar. A 2.7 mm 30° arthroscope is introduced, and the tendon sheath is

filled with saline Irrigation is performed using gravity flow.

Under direct vision, the proximal portal is made by introducing a spinal needle, and subse-

quently an incision is made into the tendon sheath (Figure 3). Instruments as a retrograde

knife, a shaver system, blunt probes, and scissors can be used. For synovectomy in patients

with rheumatoid arthritis, a 3.5 mm shaver can be used. The complete tendon sheath can be

inspected by rotating the arthroscope around the tendon.

Figure 3. (A) Marked anatomy of posterior tibial tendon of the right foot. (B) Introduction of a 2.7mm 30° arthroscope. (C) Endoscopic view of the posterior tibial tendon at introduction of the arthroscope. (D) Blunt dissection with mosquito clamp under direct vision creating a second proximal portal

94

Synovectomy can be performed with a complete overview of the tendon from the distal

portal, over the insertion of the navicular bone to approximately 6 cm above the tip of the

medial malleolus.

Special attention should be given to inspecting the tendon sheath, the posterior aspect

of the medial malleolar surface, and the posterior ankle joint capsule. The tendon sheath

between the posterior tibial tendon and the flexor digitorum longus is relatively thin: inspec-

tion of the correct tendon should always be checked. This can be accomplished by passively

flexing and extending the toes; if the tendon sheath of the flexor digitorum longus tendon is

entered, the tendon will move up and down.

When remaining in the posterior tibial tendon sheath, the neurovascular bundle is not in

danger.

When a rupture of the posterior tibial tendon is seen (Figure 4), endoscopic synovectomy

is performed and the rupture is repaired through a mini-open approach. The advantage to

start this procedure endoscopically over the standard open procedure is that localization

of the problem is made easier by exploration of the endoscopically magnified tendon, and

consequently the size of the incision for repair of the rupture can be minimized.

At the end of the procedure, the portals are sutured to prevent sinus formation.

Post-operative management consists of a pressure bandage and partial weight-bearing

for 2-3 days. Active range of motion exercises are encouraged from the first day.

ResultsIn 1997, the senior author first described tendoscopy of the posterior tibial tendon to man-

age pathology of this tendon in an anatomic study48. From 1994 to 1997, 16 procedures

were performed on 16 patients with a mean follow up of 1.1 years7. All had a history of

Figure 4. Posterior tibial tendoscopy of the right foot in a 46- year- old female patient with pain over the posterior tibial tendon. The arthroscope is in the anterolateral portal looking proximally. (A) Superficial tear of the posterior tibial tendon (asterisk). (B) Rupture demonstrated with the arthroscopic probe. (C) Repair of the rupture through a mini open repair. (P= probe; PTT= posterior tibial tendon; TS= tendon sheath)

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persistent posteromedial ankle pain for at least 6 months, with pain on palpation of the

posterior tibial tendon, positive resistance test results, and often local swelling. Five patients

underwent a diagnostic procedure after surgery, in 5 a diagnostic procedure after a fracture

was performed, a diagnostic procedure after trauma in 1, chronic tenosynovitis in 2, screw

removal from the medial malleolus in 1, and posterior ankle arthrotomy in 2 patients. No

complications were observed.

Between 1997 and 2004, we described 19 procedures in 17 patients7. Ten endoscopic

synovectomies were performed in 8 patients who had chronic tenosynovitis due to rheuma-

toid arthritis. All had a history of persistent posteromedial ankle pain, with pain on palpation

of the posterior tibial tendon, positive resistance test results, and local swelling. All patients

were first managed conservatively, and experienced temporary pain relief. All 8 patients were

diagnosed with synovitis without a tendon rupture by MRI or ultrasound. In 3 of these 8

patients, the endoscopy was combined with an arthroscopic synovectomy of the ankle or a

hallux valgus correction. In the other nine patients, tendoscopy of the posterior tibial tendon

was performed for miscellaneous reasons. Patients were allowed full weight bearing after

the operation, except for the patient who had hallux valgus correction. All were able to

actively move the ankle post-operatively.

Johnson and Strom classified tenosynovitis of the posterior tibial tendon into three stages14:

stage one tenosynovitis, where the tendon length is normal; stage two, elongated tendon

with mobile hindfoot deformity; and stage three, elongated tendon with fixed hindfoot

deformity. Myerson modified the classification by adding stage four: a valgus angulation

of the talus and early degeneration of the ankle joint32. Chow8 reported a case series of 6

patients with posterior tibial tendon synovitis who underwent an endoscopic synovectomy

for stage 1 posterior tibial tendon insufficiency. All patients reported good results.

Lui and co-workers22 described an endoscopic assisted posterior tibial tendon reconstruc-

tion for stage 2 posterior tibial tendon insufficiency, when the posterior tibial tendon has

become permanently elongated but the flatfoot deformity still is flexible. The endoscopic

technique used is similar to the one described above. Additionally, a portal is made close to

the insertion of the anterior tibial tendon, of which the medial half is cut and stripped to

the insertion with a tendon stripper. The tendon is then retrieved through the distal portal,

and the graft is transferred to the posterior tibial tendon. The construction is augmented by

side-to-side anastomosis with the flexor digitorum longus tendon, which is supplemented by

a subtalar arthroereisis with a bioabsorbable implant. Thus far only one case was described,

with a good clinical outcome.

96

3. AchiLLes teNDoscoPY

IntroductionPathology of the Achilles tendon can be divided into non-insertional and insertional prob-

lems9,38. The first type can present as local degeneration of the tendon that can be combined

with paratendinopathy. Insertional problems are related to abnormalities at the insertion of

the Achilles tendon, including the posterior aspect of the calcaneus and the retrocalcaneal

bursa. This chapter will describe the management of non-insertional tendinopathy. These can

be divided into three entities: tendinopathy, paratendinopathy, and a combination of both.

General symptoms include painful swelling typically 2-7 cm proximal to the insertion, and

stiffness especially when getting up after a period of rest.

Patients with tendinopathy can present with three patterns: diffuse thickening of the

tendon, local degeneration of the tendon which is mechanically intact, or insufficiency of the

tendon with a partial tear. In paratendinopathy, there is local thickening of the paratenon.

Clinically, a differentiation between tendinopathy and paratendinopathy can be made. Maf-

fulli and co-workers describe the Royal London Hospital test, which is found to be positive

in patients with isolated tendinopathy of the main body of the tendon: the portion of the

tendon originally found to be tender on palpation shows little or no pain with the ankle in

maximum dorsiflexion24,26. In paratendinopathy, the area of swelling does not move with

dorsiflexion and plantarflexion of the ankle, where it does in tendinopathy26,42,53. Paratendi-

nopathy can be acute or chronic.

Differential diagnoses include pathology of the tendons of the peroneus longus and brevis,

intra-articular pathology of the ankle joint and subtalar joint, degenerative changes of the

posterior tibial tendon, and tendinopathy of the flexor hallucis longus muscle must be ruled

out. MRI and ultrasound can be used to differentiate between the various forms of tendi-

nopathy17.

We normally initiate conservative management first. Modification of the activity level of the

patient is advised together with avoidance of strenuous activities in case of paratendinopathy.

Shoe modifications and inlays can be given. Physical therapy includes an extensive eccentric

exercise program, which can be combined with icing and NSAIDs27,33,34,41. Shockwave treat-

ment, a night splint, and cast immobilization are alternative conservative methods. Sclerosing

injections of neovascularisation and accompanying nerves around the Achilles tendon have

initially shown promising results. This treatment is based on the theory that neovascularisa-

tion is seen in the vast majority of patients with Achilles tendinopathy but not in pain free

normal tendons2-4,20.

If these conservative measures fail, surgery must be considered. The percentage of patients

requiring surgery is around 25%19,23,26. The technique used for operative management of

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tendinopathy depends on the stage of the disease. Local degeneration and thickening are

usually treated by excision and curettage. An insufficient Achilles tendon due to extensive

degeneration can be reconstructed. Isolated paratendinopathy can be treated by excision of

the diseased paratenon.

Open surgery has a guarded prognosis, and is associated with a higher risk of complications

than endoscopy 1,12,29. Open techniques are also associated with an extensive rehabilitation

period of 4-12 months. Therefore, recently minimally invasive techniques were developed.

Percutaneous needling of the tendon has been described, but until now no results have

been published. Testa and co-workers described a minimally invasive technique consisting of

percutaneous longitudinal tenotomies25,44, which was later optimized by adding ultrasound

control. Eighty-three percent of patients reported symptomatic benefit at the time of their

best outcome; however, the median time to return to sports was 6.5 months43.

In combined tendinopathy and paratendinopathy, the question is whether both patholo-

gies contribute to the complaints. An anatomic cadaver study described degenerative

changes of the Achilles tendon in as much as 34% of subjects with no complaints15. Khan

and co-workers only found abnormal morphology in 65% (37 of 57) of symptomatic ten-

dons, but also in 32% (9 of 28) of asymptomatic Achilles tendons assessed by ultrasound16.

Therefore, it is questionable whether degeneration of the tendon itself is the main cause of

the pain. The authors therefore focus mainly on management of the paratendinopathy leav-

ing the tendinopathy untouched. The current approach is an endoscopic release or resection

of the plantaris tendon at the level of the nodule and removal of the local paratendinopathy

tissue at the level of the painful nodule.

Surgical techniqueLocal, epidural, spinal and general anaesthesia can be used for this procedure, which can be

performed on an outpatient basis. The patient is in prone position. A tourniquet is placed

around the thigh of the affected leg, and a bolster is placed under the foot. Because the

surgeon needs to be able to obtain full plantar and dorsiflexion, the foot is placed right over

the end of the table (Figure 5).

The authors mostly use a 2.7 mm arthroscope for endoscopy of a combined tendinopathy

and paratendinopathy. This small- diameter short arthroscope yields an excellent picture

comparable to the standard 4 mm arthroscope; however, it cannot deliver the same amount

of irrigation fluid per time as the 4 mm sheath. This is important in procedures in which a

large diameter shaver is used (e.g. in endoscopic calcaneoplasty). When a 4 mm arthroscope

is used, gravity inflow of irrigation fluid is usually sufficient. A pressurized bag or pump

device sometimes is used with the 2.7 mm arthroscope.

The distal portal is located on the lateral border of the Achilles tendon, 2-3 cm distal to the

pathologic nodule. The proximal portal is located medial to the border of the Achilles tendon,

98 Figure 5. Positioning of a patient for endoscopy of the left Achilles tendon. (A) The patient is placed prone. (B, C) The affected leg is placed on a bolster and right over the end of the table. (C) The other foot is positioned so that the surgeon has sufficient working area

Figure 6. Posterior aspect of the right foot and ankle. Anatomy and portals for Achilles tendosopy are marked. (DP= distal portal, N= nodule, PP= proximal portal)

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2-4 cm above the nodule. When the portals are placed this way, it is usually possible to visual-

ize and work around the complete surface of the tendon, over a length of approximately 10

cm (Figure 6).

The distal portal is made first. After making the skin incision, the mosquito clamp is intro-

duced, followed by the blunt 2.7 mm trocar in a craniomedial direction. With this blunt

trocar the paratenon is approached, and is blindly released from the tendon by moving

around it. Subsequently, the 2.7 mm 30° arthroscope is introduced. To minimize the risk of

iatrogenic damage, the arthroscope should be kept on the tendon. At this moment, it can

be confirmed whether the surgeon is in the right layer between the deepest layer of the

paratenon and Achilles tendon. If not, now it can be identified and a further release can be

performed (Figure 7A-C).

The proximal portal is made by introducing a spinal needle, followed by a mosquito clamp

and probe. The plantaris tendon can be identified at the anteromedial border of the Achilles

tendon (Figure 7D). In a typical case of local paratendinopathy, the plantaris tendon, the

Achilles tendon, and the paratenon are tight together in the process. Removal of the local

Figure 7. Tendoscopy of the left Achilles tendon in a 52- year old female patient with combined tendi-nopathy and paratendinopathy. The 2.7 mm arthroscope is introduced through the distal portal looking proximally. (A) Adhesions of the paratenon (PAR) to the subcutaneous tissue (ST) overlying the Achilles tendon. (B) Removal of adhesions (AD) of the paratenon to the Achilles tendon (AT), looking from distal to proximal. (C) Paratenon released from the Achilles tendon. (D) Plantaris tendon (PT) running medial to the Achilles tendon (AT). (E) Release of the plantaris tendon. (F) Neovascularisation (arrows) before removal by bonecutter shaver

100

thickened paratenon on the anteromedial side of the Achilles tendon at the level of the

nodule, and release of the plantaris tendon which is often involved in the process (Figure 7E)

are the goals of this procedure. In cases where the fibrotic paratenon is firmly attached to the

lateral or posterior border of the tendon, a release in these areas is performed. Neovessels

(Figure 7F) accompanied by small nerve fibres can be found in this area and are removed with

a 2.7 mm full radius resector.

Changing portals can be helpful. At the end of the procedure it must be possible to move the

arthroscope over the complete symptomatic area of the Achilles tendon. After the procedure,

the portals are sutured.

Aftercare consists of a compressive dressing for 2-3 days. Patients are encouraged to

actively perform range of motion exercises. Full weight-bearing is allowed as tolerated.

Initially, the foot must be elevated when not walking.

ResultsThe senior author earlier described the results of 20 patients treated with an endoscopic

release for non-insertional tendinopathy combined with a paratendinopathy42. All patients

had had complaints for more than 2 years, and underwent conservative treatment for their

complaints before the indication for surgery was set. The results were analyzed with a follow

up of 2-7 years with a mean of 6 years. Sixteen patients were assessed at follow up, which

included completing of subjective outcome scores. The Foot and Ankle Outcome Score

(FAOS) and the Short Form general health survey with 36 questions (SF-36) were utilized.

There were no complications. Most patients were able to resume their sporting activities after

4 to 8 weeks. All patients had significant pain relief. The results of the subjective outcome

scores used were comparable to a cohort of people without Achilles tendon complaints.

Maquirriain and co-workers reported the outcome of 7 patients who underwent an

endoscopic release for chronic Achilles tendinopathy, with similar results. The mean score

of this group improved from 39 preoperatively to 89 post-operatively (on a scale of 0-100),

and there were no complications28. Most recently, Vega and co-workers published a modi-

fied endoscopic technique for the treatment of Achilles tendinopathy51. Pathological tissue

was endoscopically removed, and multiple longitudinal tenotomies were performed using a

retrograde knife blade. They reported a series of 8 patients with an excellent outcome, return

to their previous sports activities and no complications.

Patellar tendinopathy has a histological picture similar to that of Achilles tendinopathy.

Recently, Wilberg and co-workers have developed an arthroscopic technique for patellar

tendinopathy53. Part of their technique is comparable to Achilles tendoscopy; the main goal

is to shave the area with neovessels and accompanying nerves on the posterior aspect of the

patellar tendon, whereas this is one of the goals for endoscopic management of Achilles

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tendinopathy. A pilot study showed good clinical results in 13/15 tendons (6/8 elite athletes);

all satisfied patients were back to their previous sport activity level.

coNcLUsioNs

The results of endoscopic surgery of tendons around the ankle seem promising. More experi-

ence must be acquired by different orthopaedic surgeons. Also, accurately designed studies

need to be performed, to optimize techniques and ultimately be able to offer patients these

minimally invasive treatments with its great advantages.

102

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33. Norregaard J, Larsen CC, Bieler T, Langberg

H. Eccentric exercise in treatment of Achilles

tendinopathy. Scand J Med Sci Sports 2007;

17(2): 133-138.





Med 2004; 38(1): 8-11.

35. Paus AC. Arthroscopic synovectomy. When,

which diseases and which joints. Z Rheuma-

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36. Porter DA, Baxter DE, Clanton TO, Klootwyk

TE. Posterior tibial tendon tears in young

competitive athletes: two case reports. Foot

Ankle Int 1998; 19(9): 627-630.

37. Roggatz J, Urban A. The calcareous periten-

dinitis of the long peroneal tendon. Arch

Orthop Trauma Surg 1980; 96(3): 161-164.

38. Saltzman CL, Tearse DS. Achilles tendon

injuries. J Am Acad Orthop Surg 1998; 6(5):

316-325.

39. Scholten PE, van Dijk CN. Tendoscopy of the

peroneal tendons. Foot Ankle Clin 2006;

11(2): 415-20.

40. Schweitzer GJ. Stenosing peroneal tenovagi-

nitis. Case reports. S Afr Med J 1982; 61(14):

521-523.






Med Sci Sports 2001; 11(4): 197-206.







44. Testa V, Maffulli N, Capasso G, Bifulco G.

Percutaneous longitudinal tenotomy in

chronic Achilles tendonitis. Bull Hosp Jt Dis

1996; 54(4): 241-244.

104

45. Trnka HJ. Dysfunction of the tendon of

tibialis posterior. J Bone Joint Surg Br 2004;

86(7): 939-946.

46. van Dijk CN. Hindfoot Endoscopy. Sports

Med Arthrosc Rev 2000; 8: 365-371.

47. van Dijk CN, Kort N. Tendoscopy of the

peroneal tendons. Arthroscopy 1998; 14(5):

471-478.

48. van Dijk CN, Kort N, Scholten PE. Tendoscopy

of the posterior tibial tendon. Arthroscopy

1997; 13(6): 692-698.




1997; 5: 170-178.

50. van Dijk CN, Scholten PE, Krips R. A 2-portal

endoscopic approach for diagnosis and

treatment of posterior ankle pathology.

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51. Vega J, Cabestany JM, Golano P, Perez-Carro

L. Endoscopic treatment for chronic Achilles

tendinopathy. Foot Ankle Surg 2008; 14(4):

204-210.

52. Willberg L, Sunding K, Ohberg L, Forssblad

M, Alfredson H. Treatment of Jumper’s knee:

promising short-term results in a pilot study

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Sports Med 1993; 16(3): 216-220.

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MR findings in peroneal tendonopathy. J

Comput Assist Tomogr 1995; 19(3): 460-464.

Chapter 6

The plantaris tendon and a potential role in midportion

Achilles tendinopathy: an observational anatomical study

MN van Sterkenburg

GMMJ Kerkhoffs

RP Kleipool

CN van Dijk

J Anat 2011; 218: 336-341

108

ABstrAct

The source of pain and the background to the pain mechanisms associated with midportion

Achilles tendinopathy have not yet been clarified. Intratendinous degenerative changes are

most often addressed when present. However, it is questionable if degeneration of the ten-

don itself is the main cause of pain. Pain is often most prominent on the medial side, 2-7 cm

from the insertion onto the calcaneus. The medial location of the pain has been explained to

be caused by enhanced stress on the calcaneal tendon due to hyperpronation. However, on

this medial side the plantaris tendon is also located. It has been postulated that the plantaris

tendon might play a role in these medially located symptoms. To our knowledge, the exact

anatomy and relationship between plantaris- and calcaneal tendon at the level of complaints

have not been anatomically assessed. This was the purpose of our study. One-hundred and

seven lower extremities were dissected. After opening the superficial fascia and paraten-

don, the plantaris tendon was bluntly released from the calcaneal tendon moving distally.

Incidence of the plantaris tendon, its course, site of insertion and possible connections were

documented. When with manual force the plantaris tendon could not be released, it was

defined as a ‘connection’ with the calcaneal tendon. In all specimens a plantaris tendon

was identified. Nine different sites of insertion were found, mostly medial and fan-shaped

onto the calcaneus. In 11 specimens (10%) firm connections were found at the level of the

calcaneal tendon midportion. Clinical and histological studies are needed to confirm the role

of the plantaris tendon in midportion Achilles tendinopathy.

Ch

apter 6

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iNtroDUctioN

Midportion Achilles tendinopathy is an entity that is generally difficult to treat. Peritendinous

and intratendinous changes seem to co-exist in the majority of patients29. The source of

pain and the background to the pain mechanisms associated with midportion Achilles tendi-

nopathy have not yet been clarified17. Therefore, a wide range of conservative and surgical

treatments is available, addressing different possible contributing properties of the tendon

and its surrounding tissues. Why surgery promotes healing of the Achilles tendon is still not

understood22. Intratendinous degenerative changes are most often addressed when present.

However, it is questionable if degeneration of the tendon itself is the main cause of pain,

since intratendinous changes are found in up to 34% of people without complaints8,12,14,15.

Recently a long-term follow-up study was published revealing persistent structural abnor-

malities and thickening of the tendon 13 years after intra-tendon surgery for midportion

Achilles tendinopathy, whereas all patients were satisfied with the results and went back to

calcaneal tendon loading activities without restrictions1.

Pain is the main symptom that leads a patient to seek medical help. It is often most

prominent at 2-7 cm from the insertion onto the calcaneus on the medial side26. Most

ultrasonographic midportion disorders (91-100%) are found in this medial segment of the

tendon7,10. It has been proposed that the medial pain is caused by enhanced stress on the

calcaneal tendon due to hyperpronation. However, on this medial side the plantaris tendon

is also located. It is enclosed in a paratendon collectively with the calcaneal tendon. Steenstra

and co-workers described that during Achilles tendoscopy for patients with symptomatic

Achilles tendinopathy, the plantaris tendon was fixed to the Achilles tendon at the level of

complaints. Where in a normal situation the plantaris tendon can glide in relation to the

Achilles tendon, it was postulated that the plantaris tendon plays a role in these medially

located symptoms28.

To our knowledge, the exact anatomy and relationship between the anatomical structures

at the level of midportion calcaneal tendon complaints have not been assessed. This was the

purpose of our study.

methoDs

SpecimensOne hundred and seven lower extremities were obtained from donors. During their lives

the donors signed informed consent for the use of their bodies for scientific or educational

purposes. Twenty six were fresh-frozen (– 200) and thawed at room temperature for dissec-

tion. Eighty-one had been fixated in formalin. Sixty-two were male legs, 37 female and of 8

this information was not available. History was unknown. Mean age was 84 years (SD±9.3).

110

Fifty-three left (49.5%)-, and 54 (50.5%) right lower legs were dissected. Of 22 specimens

both legs were available (n=44), 63 were unilateral.

Anatomical dissectionDissection was done by two observers. A longitudinal incision though the skin and subcu-

taneous tissue was made from the condylus medialis femoris to the medial distal 1/3 of the

calcaneus, after which it was lengthened perpendicularly to the lateral side of the calcaneus.

After opening the superficial fascia and paratendon, the midportion of the calcaneal tendon

was inspected. Distally the plantaris tendon was not always visible; when searched for proxi-

mally after bluntly releasing the fascia between the medial belly of the gastrocnemius muscle

and the soleus muscle, it could always be identified. After this it was released by hand from

the calcaneal tendon moving distally (Figure 1).

When with maximum manual pulling force the plantaris tendon could not be released

from the calcaneal tendon, it was defined as an attachment to the calcaneal tendon. Loca-

tion of the attachment in relation to the insertion of the calcaneal tendon was measured with

a millimetre precise ruler.

Figure 1. Technique of identification of plantaris tendon (A) The skin, subcutaneous layers, superficial fascia and paratendon are dissected. (B) The plantaris tendon is identified proximally between the medial head of the gastrocnemius muscle and the soleus muscle. (C,D,E,F) With the index finger, the tendon is released to its distal insertion. Then the insertion is carefully exposed

Ch

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111

The calcaneal tendon, incidence of the plantaris tendon, their relationships and the site

of the midportion calcaneal tendon and of the insertion of the plantaris tendon onto the

calcaneus were documented.

resULts

One- hundred and seven lower legs were dissected.

In 96 specimens the calcaneal tendon and plantaris tendon run separately and can glide

in relation with each other. In the other 11 specimens we found a firm attachment of the

plantaris tendon to the calcaneal tendon; in 6 of 26 fresh frozen specimens (23%), and in 5

of 81 formalin fixated specimens. In 3 specimens the plantaris- and calcaneal tendon were

held together by a retinaculum- like structure, transversally constricting the calcaneal and

plantaris tendon 32-88 millimetres (mm) proximal to the insertion (Figure 2); in 3 specimens

the plantaris tendon inserted on the midportion of the calcaneal tendon at 20- 65 mm

proximal to the calcaneal insertion of the calcaneal tendon; two inserted into the deep

fascia; 2 adhered onto the anteromedial- and one onto the anterior side of the calcaneal

tendon by cords of solid tissue but inserted into the calcaneus. The macroscopic image of a

retinaculum-like structure made us consider this as being prone to pathology (Figure 2). Four

of 11 attachments were in legs of which the other side was also available; however, none of

the connections were bilateral.

In all specimens a plantaris tendon was identified (100%).

We found 9 different sites of insertion of the plantaris tendon, which are described and

depicted in figure 3. In only 14% of 22 paired legs (3 pairs) site of insertion on the left leg

was identical to that of the right.

Figure 2. A firm attachment between the calcaneal - and plantaris tendons at the midportion level of the Achilles tendon. This type was named ‘retinaculum-like’

112

DiscUssioN

In 11 specimens a firm connection between calcaneal - and plantaris tendon was found, at

the level of the midportion of the calcaneal tendon. This corresponds to the level at which

complaints in patients with midportion Achilles tendinopathy are present. In 3 other speci-

mens (2.8%) the plantaris tendon inserted into the calcaneal tendon. This variance has been

described before6. On the contrary, the firm connections (10%) between the plantaris- and

calcaneal tendon have not been described before. We however found connections in 10% of

our specimens. How then can we explain these findings? One way could be that these con-

nections are congenital or an anatomical variation. Another explanation could be that these

connections have developed later in life. We do not have a history of our specimens and

thus we do not know whether they were symptomatic or not. Degenerative changes in the

calcaneal tendon have been found in up to 34% of subjects without complaints1,8,12,14,15.

If peritendinous adhesions occur secondary to intratendinous changes, this can offer an

explanation for the connections and adhesions that we found. Development later on in life

Figure 3. Sites of insertion of the plantaris tendon

Ch

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Figure 4. Degree of rotation and position of the gastrocnemius-soleus complex at the midportion of the calcaneal tendon. (GC= gastrocnemius; S= soleus.) The most common (52%) position is depicted in (A), (B) occurs in 35%, and (C) in 13%. In all situations, the soleus fibres are positioned medially. The location of the plantaris tendon is shown (PT) (Illustration as adapted from Cummins and co-workers4)

seems to be the most likely explanation of this high percentage of a firm connection between

the plantaris- and calcaneal tendon at the midportion level.

Now could these connections between calcaneal-and plantaris tendon explain the medial

pain in midportion Achilles tendinopathy? We aimed to theorize this by applying anatomical

and pathophysiological evidence.

The calcaneal tendon consists of the fibers of two muscle units in the superficial compart-

ment of the posterior leg: the gastrocnemius muscle (medial and lateral head) and the soleus

muscle. The gastrocnemius muscle crosses the knee and ankle joints (ankle and subtalar);

originating from the posterior surface of condylus medialis and -lateralis femoris and insert-

ing onto the calcaneus. The soleus muscle lies anterior to the gastrocnemius muscle and

originates from each side of the anterior aponeurosis attached to the tibia and fibula, and

from the posterior surfaces of the head of the fibula and its proximal quarter, as well as the

middle third of the medial border of the tibia. The soleus muscle only crosses the 2 ankle

joints. Distally, both the gastrocnemius and soleus muscles form an aponeurosis, from each

of which a tendon originates. At about the level where the soleus contributes fibers to the

calcaneal tendon, rotation of the tendon begins and becomes more marked in the distal 5-6

cm. The gastrocnemius fibers rotate to lateral and the soleus fibers are positioned medial to

the insertion20. This anatomical observation means that the medial portion of the calcaneal

tendon, where pain is often most prominent, is bi-articular since it consists of fibers originat-

ing from the soleus muscle (Figure 4). The calcaneal tendon is involved in plantarflexion,

whereas according to its anatomical course, the tri-articular plantaris tendon also contributes

114

to ankle inversion. These opposite forces result in an intermittent small change of position

between calcaneal - and plantaris tendon which occurs with every step.

Unlike other tendons in the leg, the Achilles tendon lacks a synovial sheath. Instead, it has a

paratendon, which is an array of thin, fibrous tissue containing blood vessels23. In patients

with symptomatic Achilles tendinopathy, enhanced neurovascular growth from the para-

tendon into the calcaneal tendon in an attempt to repair the tendon proper is seen. Also

myofibroblasts responsible for the formation of permanent scarring and the shrinkage of

peritendinous tissue have been shown. The plantaris tendon runs with the calcaneal tendon

inside a collective paratendon. With the development of scarring and shrinkage of periten-

dinous tissue, the calcaneal - and plantaris tendon will adhere. The opposite movements

between plantaris- and calcaneal tendon will result in traction to the firm peritendinous tissue

that connects both tendons and the level of the tendinopathy. This tissue has recently been

described to be richly innervated by neonerves which may be involved in causing pain2,24.

Pain then aggravates with movement, given the fact that the traction forces occur with every

step with an average of 5,000 - 12,500 steps/ day30,31.

There are 2 drawbacks to our study. Histological examination would have provided us with

more information on the nature of the connections, and is necessary to gain more relevant

data for conclusions concerning a potential role in midportion Achilles tendinopathy. Another

drawback is the fact that age and former lifestyle of our specimens did not match with the

group of active 30 to 50 year-olds in which midportion Achilles tendinopathy most often

occurs.

The consequences of formalin fixation are yet unknown. It may alter the properties of

soft tissue structures, making blunt division of calcaneal- and plantaris tendons easier, con-

sequently missing possible connections. We found 23% of connections in fresh-frozen but

only 6% in formalin- fixated specimens. Larger numbers of specimens may be needed to

substantiate this finding. Dissection of exclusively fresh frozen specimens might have been

beneficial since this may be the closest we can get to in vivo tissue texture.

A strinking finding was that, as opposed to the widely accepted rule that in a large sample of

patients a number of plantaris muscles/tendons is missing, in all our 107 specimens a plan-

taris tendon was identified. According to previous anatomical studies with large numbers of

specimens, the plantaris tendon is absent in a number of cases (7-20%)5,6,9,11,19,25. Daseler

found in 542 pairs of legs that in 9 the right plantaris tendon was absent, and in 21 the left.

Moreover, in 31 pairs the plantaris muscle could not be identified. Harvey and co-workers

noted the absence of plantaris in 18.2% of 658 lower limb dissections13.

These earlier findings of absence in anatomical studies could be attributable to the tech-

nique of dissection. In our 5 cases where the tendon inserted into the calcaneal tendon,

Ch

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115

Figure 5. (A) Anatomical course of the plantaris tendon according to Sobotta Anatomy; (B) course found during 107 dissections

anterior to the tendon on the calcaneus and in the crural fascia (4.6%), the plantaris

tendon could not be identified distally (Figure 3). We started our dissection between the

gastrocnemius and soleus muscles (Figure 1), and identified a plantaris tendon in all our

specimens. Unfortunately only two studies specified their dissection techniques. Freeman

and co-workers (13% absence) specifically aim for the muscle belly dissecting the proximal

dorsal compartment of the lower leg; Harvey (18.2% absence) mentions not dissecting the

lower legs all the way to proximal13. With our relatively large group of specimens, we not

only contradict earlier findings of its absence, but also raise implications for daily practise.

The plantaris tendon is often used for grafting because it can be sacrificed without markable

deficit, and is of adequate length and thickness for most applications3,16,18,27. It is often

excised from distally. In this case it will be missed in a substantial number of cases. We advise

to retrieve it more proximally (e.g. with a tendon stripper). Using ultrasound- or MR- imaging

prior to surgery to pre-assess its course may be helpful.

Another discrepancy with the existing knowledge was the mid-course of the plantaris tendon

in the posterior compartment of the lower leg.

According to Sobotta Anatomy21, the plantaris tendon instantly crosses the posterior side

of the calf, to run medial with the calcaneal tendon until its insertion (Figure 5). In our

observations the plantaris tendon along its course gradually crosses the calf between the

gastrocnemius and the soleus muscle.

116

With this study we can theorize but not confirm that the plantaris tendon plays a role in

complaints in patients with midportion Achilles tendinopathy. However, we do know more

about the course and insertion of the plantaris tendon. Interesting and unexpected find-

ings were the firm connections between plantaris- and calcaneal tendon at the level of in

midportion of the calcaneal tendon in 10% of specimens. Clinical studies on the outcome

of surgically removing plantaris tendons and thereby severing adhesions and accompanying

enhanced neurovascular growth from the paratendon at the medial side of the calcaneal

tendon may provide us with more evidence on the relation between the plantaris tendon and

symptomatic midportion Achilles tendinopathy.

AckNowLeDGemeNts

The authors would like to thank the Department of Anatomy & Embryology, particularly Mrs.

C.G.J. Cleypool, and the Department of Pathology for facilitating the dissections.

Ch

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Chapter 7

Good outcome after stripping the plantaris tendon in patients

with chronic midportion Achilles tendinopathy

MN van Sterkenburg

GMMJ Kerkhoffs

CN van Dijk

Knee Surg Sports Traumatol Arthrosc 2011;19:1362-1366

122

ABstrAct

PurposeAchilles tendinopathy is a problem that is generally difficult to treat. The pain is frequently

most prominent on the medial side of the midportion of the tendon, where the plantaris

tendon is running parallel to the Achilles tendon. The purpose of this study was to assess if

excision of the plantaris tendon would relieve symptoms.

MethodsThree patients with pain and stiffness at the midportion of the Achilles tendon were treated

by excision of the plantaris tendon. Pre-operatively these patients experienced recognisable

tenderness on palpation of the medial side of the midportion of the Achilles tendon with

localized nodular thickening at 4-7 cm proximal to the insertion. MRI indicated Achilles

tendinopathy with involvement of the plantaris tendon.

ResultsThe plantaris tendon was bluntly retrieved and excised with a tendon stripper through a 3 cm

incision in the proximal calf. We report a good to excellent outcome of this novel procedure

in 3 patients with chronic midportion Achilles tendinopathy.

ConclusionThe medial pain might be based on involvement of the plantaris tendon in the process.

Ch

apter 7

Go

od

ou

tcom

e after stripp

ing

the p

lantaris ten

do

n in

patien

ts with

chro

nic m

idp

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n A

chilles ten

din

op

athy

123

iNtroDUctioN

Midportion Achilles tendinopathy is generally difficult to treat. The source of pain and the

background to the pain mechanisms associated with it have not been scientifically clarified15.

Isolated symptomatic tendinopathy is rare, most often the paratenon is involved28. A wide

range of conservative and surgical treatments is available. The role of surgery is still not

fully understood22. Most operative procedures are directed at the Achilles tendon itself. The

intratendinous degenerative changes are incised or excised. It is questionable however if

degeneration of the tendon itself is the main cause of the pain in midportion tendinopathy.

Morphologic and degenerative changes in the Achilles tendon seem to be a part of aging

and in many cases there is no correlation with symptoms25,29. Several studies have reported

intratendinous changes in up to 34% of cadaver specimens, ultrasound- and MRI images of

patients without complaints6,7,9,10,30. Recently a long-term follow-up study was published by

Alfredson et al. revealing persistent structural abnormalities and thickening of the tendon 13

years after intratendinous surgery for Achilles tendinopathy, whereas all patients were satis-

fied with the results and went back to Achilles tendon loading activities without restrictions1.

In patients with a painful nodular thickening in the Achilles tendon, the pain is often most

prominent on the medial side of the midportion Achilles tendon24. At this level the plantaris

tendon runs closely with- and parallel to the Achilles tendon. An inflammatory response of

the paratenon (located around the Achilles- and plantaris tendon) at the level of the painful

nodule may result in adhesions between plantaris- and Achilles tendon. We hypothesize that

the medial pain may be caused by these adhesions. If this hypothesis were to be correct,

isolated stripping or release of the plantaris tendon would be sufficient to relieve complaints.

This paper reports on a novel technique of isolated stripping of the plantaris tendon in 3

patients with chronic midportion Achilles tendinopathy.

methoDs

Three consecutive patients with midportion tendinopathy of the Achilles tendon were

included (2 female, 1 male). Mean age was 47 years (43, 48, and 50). Patients had complaints

of pain and stiffness of the Achilles tendon for a mean of 32 months (11, 37 and 48), with

a palpable painful nodule 4, 6, and 7 centimetres proximal of the insertion of the Achilles

tendon onto the calcaneus. In all 3 patients pain on palpation was predominantly on the

medial side. Conservative treatment had failed and none had had previous hindfoot surgery.

Magnetic Resonance Imaging (MRI) confirmed the clinical diagnosis of Achilles tendinopathy

with involvement of the plantaris tendon in this process.

Visual Analogue Scales (VAS) for pain and function19 and Victorian Institute of Sports Assess-

ment –Achilles (VISA-A) questionnaires20 were filled out by all three patients pre-operatively,

124

6 weeks and 1 year postoperatively. Additionally time to- and level of sport resumption, as

well as 4 point scales for satisfaction (bad, poor, good, excellent) and complaints (more,

same, less, none) were documented.

Surgical procedure The procedure was performed under general or spinal anaesthesia. The patients were placed

in the prone position. A tourniquet was applied. A 4 cm posteromedial incision was made in

the proximal third of the calf. The plane dividing the medial belly of the gastrocnemius muscle

and the soleus muscle was retrieved by blunt dissection. This is where the plantaris tendon

runs in this plane from the posterolateral femoral condyle to the medial calcaneus. The

plantaris tendon was identified, released, and pulled medially for visualization through the

incision. After placing holding sutures, the tendon was transsected and threaded through a

tendon stripper. The stripper was advanced slowly with the leg fully extended, until it passed

the palpable nodule (Figure 1). Then the plantaris tendon was cut distally and removed

Figure 1. Surgical technique. (A) A 4-5 cm incision is made. The plantaris tendon is bluntly identified.and pulled medially for visualization through the incision. (B) A holding suture is placed. (C) The tendon is transsected and threaded through a tendon stripper. (D) The stripper is advanced slowly with the leg fully extended. When the calcaneus is reached the tendon is cut

Ch

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125

Figure 2. Result; right is the distal portion of the Achilles tendon removed past the adhesions, left (with holding suture) the proximal portion

through the proximal incision (Figure 2). The superficial fascia, subcutaneous tissues and skin

were closed. Aftertreatment consisted of a compression bandage for 2 days. Weight- bearing

was allowed as tolerated.

resULts

All three patients were scheduled for the surgical procedure as explained above. Pre-

operatively VAS for pain was 69, 58 and 59 (mm) respectively. VAS for function was only

taken from case 2 and 3, being 16 and 24 (mm). Pre-operative VISA-A-NL scores were 19,

25 and 45 points.

The first case had a large lower leg for which the stripper was too short, so it was decided

to convert. At the level of the nodule a 3 cm medial longitudinal incision was made and

the superficial fascia was opened. The paratenon was longitudinally dissected. The plantaris

tendon could not be identified at this level because of extensive adhesions. After lengthening

the incision 3 cm to proximal the plantaris tendon came into view. It was cut proximally,

bluntly released distal from the process and resected. Six weeks after the procedure VAS for

pain was 13 (mm), - for function 64 (mm), the VISA-A-NL score measured 64 points. There

were less complaints and a good outcome. After 4 weeks he had resumed sporting activities,

but still on a lower level. At one year follow-up, VAS for pain was 3 (mm), VAS for function

92 (mm) and VISA-A-NL 97. There were no complaints and excellent outcome playing sports

after 6 weeks at a higher level than pre-operatively.

The second case went without technical problems. The plantaris tendon was histologically

examined and showed signs of chronic inflammation. Six weeks postoperatively she had less

complaints and an excellent subjective outcome. VAS for pain was 17 (mm), - for function 78

(mm) and VISA-A-NL measured 55 points. After one year she reported less complaints and

excellent outcome, with VAS for pain of 4 (mm), for function 95 (mm) and VISA-A-NL 55. As

the VISA-A accredits 45 out of 100 points to sports, this patient could not score higher than

55 points as she was not sports active.

In the third case, the connection between Achilles- and plantaris tendon was so tight

that the stripper could not pass the process and the plantaris tendon ruptured proximal to

this process. It was decided to end the procedure. Histology obviously showed no signs of

pathology. On 6 weeks follow- up she had less complaints and was moderately satisfied with

126

the surgery. VAS for pain measured 0 (mm), for function 98 (mm), and VISA-A-NL scored

77 points. She resumed her sporting activities after 6 weeks at the same level as before

complaints. After one year she reported no complaints and a good outcome with VAS for

pain of 0 points (mm), - for function 100 (mm) and VISA-A-NL outcome of 91 points.

DiscUssioN

The most important finding of our study was that all patients had a good outcome with strip-

ping of the plantaris tendon only. A new surgical technique to relieve symptoms in patients

with midportion Achilles tendinopathy with pain predominantly located on the medial side

of the Achilles tendon is reported. Involvement of the plantaris tendon in the pathological

process was confirmed on MRI.

How can removal of this possibly rudimentary plantaris tendon relieve the often recalci-

trant complaints? The plantaris tendon lies posterior to the knee joint, originating from the

inferior part of the lateral supracondylar line of the femur. Its tendon travels inferomedially,

posterior to the soleus muscle and anterior to the medial gastrocnemius muscle. The tendon

crosses the calf relatively proximal, running medial from, and parallel with the Achilles tendon

from the midportion of the calf; in the majority of cases ultimately inserting medially onto

the calcaneus5, 8. The plantaris muscle-tendon complex is a weak ankle- and knee flexor and

ankle invertor. Additionally, the medial portion of the Achilles tendon consists solely of the

soleus tendon since at about the level where the soleus contributes fibers to the Achilles

tendon, rotation of the tendon begins. Gastrocnemius fibers are therefore positioned lateral-

and soleus fibers medial of the insertion. The soleus is biarticular (ankle- and subtalar joints).

The plantaris tendon runs medial to it.

In a healthy situation the plantaris tendon can move freely in relation to the Achilles

tendon, however an inflammatory response of the paratenon may cause adhesions between

plantaris- and Achilles tendon. Adhesions cause the mechanical problem of obstruction as

the plantaris muscle-tendon complex not only causes flexion but also inversion, whereas the

triceps surae is a flexor only. Although the movement between the two is limited, traction

onto the surrounding paratenon will take place with every step. Chronic painful tendons

have been shown to exhibit new ingrowth of sensory nerve fibers from the paratenon12,23.

Repetitive traction onto this richly innervated area might explain the pain and stiffness during

and after walking. On the basis of this theory, symptom relief in our 3 cases is probably

caused by discontinuing the proximally directed drawing forces of the plantaris tendon from

its distal adhesion onto the Achilles tendon.

Another explanation for the pain relief might be ‘denervation’. As seen in studies on various

species, it is shown that the nerves to the Achilles tendon have in part a cutaneous origin,

including the sural nerve, and an origin from the associated muscles2,3,27. The healthy Achilles

Ch

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tendon proper is superficially innervated by the paratenon, but does not seem to have a rich

nervous supply itself2. The healthy tendon proper is normally aneuronal; conversely chronic

painful tendons have been shown to exhibit new ingrowth of sensory nerve fibers from the

paratenon into the tendon proper12,23. Can pain yet originate from the Achilles tendon itself

or is it caused by this nerve ingrowth from the paratenon2?

With many surgical procedures for recalcitrant Achilles tendinopathy of the tendon proper

the paratenon is released or removed. In open surgical debridement of the tendon proper the

paratenon has to be opened11,14,21, and during minimally invasive tenotomy the paratenon is

also addressed. Paratendinopathy and tendinopathy often co-exist, but in some procedures

only the peritendinous structures are addressed, such as in open or minimally invasive parate-

nectomy13,18 and Achilles tendoscopy17,26. These procedures all render good to excellent

results in 75-100% of patients. The pain relief can probably be explained by destruction of

these sensory nerves running from the paratenon into the Achilles tendon proper. When

stripping the plantaris tendon, the paratenon is also being released since plantaris- and

Achilles tendon run together within one paratenon. If pain can be relieved which isolated

release of the paratenon, surgery of the tendon proper and consequently major tendon

reconstruction becomes redundant. The advantages of a minimal invasive approach are clear

and consist of decreased peri- operative morbidity, decreased duration of hospital stay, and

reduced costs4,13,16.

There are two major limitations to our study. To advocate this technique for everyday

practise more patients are needed. The technique also needs to be optimized, e.g. the plan-

taris tendon should be identified more distally (but still proximal from the nodular thickening

in the Achilles tendon) or a longer tendon stripper is needed to avoid conversion of the

technique as in case 1.

coNcLUsioN

A good to excellent outcome of stripping tendon in 3 patients with chronic midportion Achil-

les tendinopathy is reported. The medial location of pain at physical examination might be

based on involvement of the plantaris tendon in the process. More patients and optimization

of the surgical procedure are needed to advocate this technique for everyday practise and to

support this novel approach to the pathogenesis of chronic midportion Achilles tendinopathy.

128

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4. Carmont MR, Maffulli N. Less invasive Achil-

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22. Sandmeier R, Renström PA. Diagnosis and



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24. Segesser B, Goesele A, Renggli P. The Achil-

les tendon in sports. Orthopade 1995; 24(3):

252-267.

25. Smith RK, Birch HL, Goodman S, Heinegard

D, Goodship AE. The influence of age-

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27. STILWELL DL, Jr. The innervation of tendons

and aponeuroses. Am J Anat 1957; 100(3):

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28. Tan SC, Chan O. Achilles and patellar

tendinopathy: current understanding of

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tendon. Scand J Med Sci Sports 1997; 7(2):

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30. van Schie HT, de Vos RJ, de JS et al. Ultraso-

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2010; 44(16): 1153-1159.

Chapter 8

Midportion Achilles tendinopathy: why painful?

An Evidence-based philosophy

MN van Sterkenburg

CN van Dijk

Knee Surg Sports Traumatol Arthrosc 2011;19:1367-1375

132

ABstrAct

Chronic midportion Achilles tendinopathy is generally difficult to treat as the background to

the pain mechanisms has not yet been clarified. A wide range of conservative and surgical

treatment options are available. Most address intratendinous degenerative changes when

present, as it is believed that these changes are found responsible for the symptoms. Since

up to 34% of asymptomatic tendons show histopathological changes, we believe that the

tendon proper is not the cause of pain in the majority of patients. Chronic painful tendons

show ingrowth of sensory- and sympathetic nerves from the paratenon with release of noci-

ceptive substances. Denervating the Achilles tendon by release of the paratenon, is sufficient

to cause pain relief in the majority of patients. This type of treatment has the additional

advantage that it is associated with a shorter recovery time when compared to treatment

options that address the tendon itself. An evidence- based philosophy on the cause of pain

in chronic midportion Achilles tendinopathy is presented.

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iNtroDUctioN

Chronic Achilles tendon pathology is one of the most frequent injuries in sports involving

running and jumping. In elite long-distance runners there is a lifetime risk of 52% for sustain-

ing an Achilles tendon injury39. Thirty percent of patients have a sedentary lifestyle7.

Chronic midportion Achilles tendinopathy78 is characterized by impaired performance due

to Achilles tendon pain and swelling located typically at 2-7 cm from the insertion onto the

calcaneus48. The source of pain and the background to the pain mechanisms associated with

midportion Achilles tendinopathy have not yet been clarified49. Many different explanations

have been raised. Consequently, a wide range of conservative and surgical treatment options

are available. Most of them address the intratendinous degenerative changes when pres-

ent. Surgical measures include open excision of degenerative tendon. This means that the

intratendinous changes are found responsible for the symptoms. But does the origin of the

pain in these patients indeed rise from the Achilles tendon itself? It is known that the tendon

itself is relatively aneuronal. It is also recognized that intratendinous degenerative changes

often occur without symptoms.

It is hypothesized that the main cause of the pain in patients with symptomatic midpor-

tion Achilles tendinopathy does not arise from the tendon proper but is generated by its sur-

rounding tissues. In this paper, a premise on the cause of pain based on existing knowledge

and personal research is presented.

ANAtomY

The Achilles tendon is the combination of tendons of soleus and gastrocnemius muscles,

inserting approximately halfway the calcaneus. The gastrocnemius muscle crosses the knee,

subtalar and ankle joints; originating from the posterior medial and lateral femoral condyles

and inserting onto the calcaneus. The soleus muscle lies anterior to the gastrocnemius

muscle and originates from the proximal tibia, fibula and interosseous membrane and crosses

the ankle and subtalar joints. Distally, both the gastrocnemius and soleus muscles form an

aponeurosis, from each of which a tendon originates. At about the level where the soleus

contributes fibres to the Achilles tendon, rotation of the tendon begins and becomes more

marked 2-7 cm proximal to the insertion onto the calcaneus. The gastrocnemius fibres rotate

to lateral and the soleus fibres are positioned medial to the insertion9,21,57. Medial to the

Achilles tendon the plantaris tendon is located, originating from the lateral femoral condyle

and inserting onto the medial calcaneus. The Achilles tendon is involved in plantarflexion,

whereas according to its anatomical course, the tri-articular plantaris tendon also contributes

to ankle inversion.

134

The Achilles and plantaris tendon are collectively surrounded by a paratenon, which lies

on an inner layer of endotenon, and exists of a layer of mesotenon and an outer layer of

epitenon.

Tendon consists predominantly of extracellular tissue with low metabolic requirements,

and therefore appears white on macroscopic inspection. This relatively bradytrophic char-

acter enables the tendon to remain under tension for a long period, without the risk of

necrosis or ischemia. The Achilles tendon has 3 sources of vascular supply, which are (1) the

perimyseal vessels at the musculotendinous junction; (2) periosteal vessels at the osteotendi-

nous junction; and (3) vessels around the tendon within the paratenon, forming a capillary

loop system. This last system is the main vascular supply for the Achilles tendon. The neural

supply to the Achilles tendon and the surrounding paratenon is provided by nerves from

the attaching muscles and by small fasciculi from cutaneous nerves, in particular the sural

nerve9,71. The number of nerves and nerve endings is relatively low, and the tendon proper

is relatively aneuronal43,65.

AetioLoGY

A distinction is made between the aetiology of intratendinous degenerative changes and

the aetiology of complaints in patients with midportion Achilles tendinopathy. Causes of

intratendinous changes can be divided into extrinsic and intrinsic factors, but most com-

monly will be a combination of both. Malalignment of the foot, hyperpronation63,68, age45

and chronic disease like diabetes mellitus, obesity and hypertension28 have been described.

Malalignment and hyperpronation impose excessive strain on the Achilles tendon. The aging

tendon loses its elastic properties causing the muscle to work more, resulting in a local rise in

temperature with subsequent tendon changes68.

Inappropriate physical training may also be an important issue37,46 causing degenerative

Achilles tendon changes. Tendons transmit muscle forces to bone, allowing locomotion and

enhancing joint stability. They respond to mechanical forces by changing their metabolism

and their structural and mechanical properties. Appropriate training increases the diameter

and tensile strength of tendons, with tendon fibroblasts increasing the production of collagen

type I42,53,72,75. Training also induces biochemical changes in tendons. Strenuous endurance

training increases collagen turnover and decreases collagen maturation in tendons; exces-

sive mechanical loading is considered a major concern. Repetitive strains below the failure

threshold of the tendon cause tendon micro- injuries38,61. Quality of foot gear and training

surface influencing the alignment and statics of the ankle are also often mentioned as a

cause of intratendinous pathology.

The aetiology of the pain in a patient with midportion Achilles tendinopathy has not

yet been entirely clarified. Pain was believed to be caused by expansion of the Achilles

tendon proper due to increased ground substance and an increased concentration of

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glucosaminoglycans (GAGs). A few years ago the presence of neovascularisation around

symptomatic tendons was raised as the cause of pain; now accompanying nerves with high

concentrations of nociceptive substances (glutamate, substance P, calcitonin gene related

peptide (CGRP)) are also supposed to play a role5,8.

cLiNicAL PreseNtAtioN

Symptoms of a patient with midportion Achilles tendinopathy include painful swelling

typically 2-7 cm proximal to the insertion, and stiffness especially when getting up after a

period of rest. Pain is the main symptom in Achilles tendinopathy that leads a patient to seek

medical help. It is often most prominent 2-7 cm from the insertion onto the calcaneus on the

medial side67. Tendinopathy and paratendinopathy often co-exist64. Intratendinous changes

most often remain asymptomatic35. In these cases a painless swelling at 2-7 cm proximal

to the insertion is the only finding58. In isolated paratendinopathy, there is local thickening

of the paratenon. The area of swelling does not move with dorsiflexion and plantarflexion

of the ankle, where it does in isolated tendinopathy50,69,82. Paratendinopathy can be acute

or chronic. Acute isolated paratendinopathy manifests itself as painful peritendinous crepi-

tus as the tendon glides within the inflamed covering. Areas of increased erythema, local

heat, and asymptomatic palpable tendon nodules or defects may also be present at clinical

examination. In chronic paratendinopathy, exercise-induced pain is the main symptom while

crepitation and swelling diminish.

histoPAthoLoGY

Normal situationMorphologically, healthy tendon is a complex composite material consisting of collagen fibrils

embedded in a matrix of proteoglycans, with a relative small number of cells. Between the

parallel collagen bundles, fibroblasts are arranged, which are the predominant cells within

tendons10. The matrix has tight bundles of long strands of type I collagen, which give the

tendon its inherent strength. Between the collagen is the ground substance, made up of

mainly small proteoglycans and glycosaminoglycan (GAG) chains. In normal tendon, there is

minimal ground substance14.

The paratenon consists of straight bundles of type I and type III collagen fibrils with

straight microfibrillar arrangement and variable diameter23,41. This peritendinous tissue is

lined on its inner surface by synovial cells31,82 and acts as an elastic sleeve permitting the

movement of tendon against the surrounding tissues34. The paratenon serves to carry blood

vessels, lymphatics and nerves.

136

Pathological situationIn contrast with the white appearance of healthy tendon, in tendinopathy they macroscopi-

cally appear grey or yellow-brown and amorphous. Microscopically the tendon shows dis-

rupted collagen, a decrease in the amount of type I collagen and an increase of the amount

of the weak type III collagen which is produced in response to injury and is less able to

bundle. The classical hierarchical structure is lost, there is increased ground substance with a

high concentration of GAGs, more prominent and numerous tenocytes without their normal

fine spindle shape and with more rounded nuclei14,24. Some areas of tendinopathy become

acellular36 or have decreased cell numbers and function14,33.

In the peritendinous tissue in the chronic phase of Achilles tendinopathy 2 types of cells

have been identified: fibroblasts and myofibroblasts41. During biological processes that include

extensive tissue remodelling, fibroblasts may acquire morphological and biochemical features

of contractile cells which have been named myofibroblasts20. The myofibroblasts have stress

fibers composed of α–smooth muscle actin in their cytoplasm and thus are capable of creat-

ing forces required for wound contraction20. In chronic Achilles tendinopathy, these cells are

especially well established at the sites of scar formation, and it is estimated that about 20%

of peritendinous cells are myofibroblasts41. The myofibroblasts synthesize abundant amounts

of collagen and are believed to be responsible for the formation of permanent scarring and

the shrinkage of peritendinous tissue around the tendon30,41. They can induce and maintain

a prolonged contracted state in the peritendinous adhesions around the tendon and thus

influence the development of a contracture30,41. This, in turn may lead to constriction of

vascular channels and to impaired circulation and further contribute to the pathogenesis of

Achilles tendinopathy. The proliferating connective tissue around the Achilles tendon causes

increased intratendinous tension and pressure resulting in increased friction between the

tendon, paratenon, crural fascia, and the skin30.

Vascularity seems increased in tendinopathy, as neovascularisation with thick walls, a

tortuous appearance and small lumen ventral from the Achilles tendon and in the paratenon

is found in 50-88% of symptomatic tendons but not in pain- free tendons18,59,60,80,83.

The healthy Achilles tendon proper is superficially innervated by the paratenon, but

does not have a rich nervous supply itself8. It is normally aneuronal; conversely chronic

painful tendons have been shown to exhibit new ingrowth of nerve fibers accompanying

the peritendinous neovascularisation from the paratenon into the tendon proper43,65. Sen-

sory nerve ingrowth has been observed as a reaction to repetitive loading52 and also as a

response to injury2,4. With this nerve ingrowth, levels of glutamate, calcitonin gene-related

peptide (CGRP) and substance P rise4,8,43,65. These substances are all linked with increased

nociception. Substance P is also associated with vasodilation and stimulates proliferation of

fibroblasts70, possibly causing some of the morphologic changes in Achilles tendinopathy.

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Figure 1A-C. (A) Schematic depiction of normal tendon. (B) Pathological tendon proper. (C) Vasculoneuronal ingrowth from the paratenon into the tendon proper

cAUse of PAiN

Several factors play a role in the cause of pain in a patient with Achilles tendinopathy.

The process starts with localized tendon micro- injury and degeneration which are caused

by ageing and repetitive strain below the failure threshold of the tendon. The most hypovas-

cular region is in the midportion area (2-7 cm from the insertion), where the tendon makes

a marked twist. This is the location where the degeneration and micro-injury most often

occur. Blood flow further declines with ageing and mechanical loading. When the demands

of the tendon are higher than can be managed, micro-injuries develop1. The body reacts

with a repair process, which is adequate in most cases, but inadequate in patients developing

tendinopathy. This inadequate repair causes a repetitive cycle of inadequate collagen and

matrix production, tenocyte disruption, a further decrease of collagen and matrix and an

increased vulnerability to further micro-injuries. Due to the lack of bloodvessels within the

tendon, instead of a chemical- a neurogenic inflammatory process is activated to repair these

microruptures. This neurogenic inflammation occurs in the tissue surrounding the Achilles

tendon. Matrix metalloproteinases (MMPs) responsible for the degradation of extracellular

matrix, cytokines (vascular endothelial growth- factor (VEGF), epidermal growth factor (EGF),

and platelet- derived growth factor (PDGF)) are over- expressed. VEGF promotes angiogen-

esis, upregulates the expression of MMPs and down-regulates tissue inhibitors of metal-

loproteinases (TIMP-3), altering the properties of tendon. Invasion of vessels derived from the

paratenon into a normally hypovascular intratendinous region weakens the normal tendon

structure. When the repair of tendon is inadequate, e.g. due to submission to further loads

without adequate recovery time or a declined blood flow due to ageing, the healing process

fails and the pathogenic cascade leading to symptomatic tendinopathy occurs. The transition

to symptomatic tendinopathy is marked by nerve proliferation accompanying the neovessels.

Vascular ingrowth to repair the defect arises from the paratenon. These bloodvessels are

accompanied by sensory neonerves11,22 (Figure 1), causing an increase in pain signalling by

138

producing nociceptive substances (glutamate, substance P, calcitonin gene related peptide

(CGRP)) past the critical threshold5,8. Neovascularisation has indeed been found to correlate

with the location of pain in patients with symptomatic tendinopathy19. The upregulated

nociceptive substances further damage the tendon by inducing vasodilation, tendon cell

apoptosis and the vicious circle of neurogenic inflammation1,5,8,22,54.

Myofibroblasts proliferate and are transported by the peritendinous blood vessels and neo-

vascularisation into the peritendineum and the tendon proper. Myofibroblasts synthesize

abundant amounts of collagen to repair the tendon proper, but also cause the formation

of scar tissue around the tendon and consequently adhesions of the paratenon onto the

Achilles tendon at the location of the neurovascular ingrowth. Scarring in turn may lead

to constriction of vascular channels and to impaired circulation and further contribute to

the pathogenesis of Achilles tendinopathy, meaning that there is no further action towards

repair.

Vasoconstriction and scarring with mechanical constriction will lead to obliteration of

neovessels. In 20-50% of long lasting tendinopathy patients no neovascularisation is

Figure 2A-D. (A) Adhesion of the paratenon onto the Achilles tendon due to myofibroblast prolif-eration and consequently formation of scar tissue. (B) Continuing ingrowth of vessels and nerves and augmented adhesion (C) Obliteration of neovessels due to constriction. (D) The painful end situation in which neovascularisation has been mostly obliterated but nerve endings persist

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Figure 3. The most common position (52%) of the gastrocnemius-soleus complex at the midportion of the Achilles tendon 15 (PT= plantaris tendon, S= Soleus, GC= Gastrocnemius)

found18,59,60,80,83. Nerves however will survive (Figure 2), secreting glutamate and substance

P causing pain on activity as described earlier.

Reduction of blood flow may also be explained by the fact that pathological tendons exhibit

a decreased occurrence of sympathetic nerve fibres. This reduction in vasoregulatory nor-

adrenalin causes vasoconstriction3.

It has been described that the location of the pain in patients with Achilles tendinopathy is

most often located on the medial side67,69. During Achilles tendoscopy in patients with Achil-

les tendinopathy, it has been observed that at the level of complaints the plantaris tendon

is affixed onto the Achilles tendon on the medial side69 (Figure 3). Some authors describe a

higher medial stress onto the Achilles tendon due to hyperpronation. This is supported by the

finding that most ultrasonographic midportion disorders (91%) are found in the (postero)-

medial segment of the tendon26,79.

In patients with a painful nodular thickening in the Achilles tendon, the pain is often most

prominent on the medial side of the midportion Achilles tendon. At this level the plantaris

tendon runs closely with- and parallel to the Achilles tendon.

The plantaris tendon originally is a knee -and ankle flexor. In primates it attaches to the

plantar aspect of the proximal interphalangeal joints of the toes in primates, explaining its

functionality for grasping with their feet. Darwinists suggest that through evolution in humans

140

the plantaris tendon is rudimental since human beings do not grasp with feet nor swing from

trees any longer. Absence in 7-20% human lower limbs has been reported16,17,25,55,66.

In humans the plantaris muscle is triangularly shaped and lies posterior to the knee joint,

originating from the inferior part of the lateral supracondylar line of the femur. Its tendon

travels inferomedially, posterior to the soleus muscle and anterior to the medial gastroc-

nemius muscle. The tendon crosses the calf relatively proximal, running medial from, and

parallel with the Achilles tendon from the midportion of the calf; in the majority of cases

ultimately inserting medially onto the calcaneus17,27. The plantaris muscle-tendon complex

nowadays is a weak ankle- and knee flexor and ankle invertor.

The medial portion of the Achilles tendon consists solely of the soleus tendon since at

about the level where the soleus contributes fibers to the Achilles tendon (3-11 cm), rotation

of the tendon begins and becomes more marked in the distal 5-6 cm. Gastrocnemius fibers

are therefore positioned lateral- and the soleus fibers on the medial side of the insertion

(Figure 4). The soleus is biarticular (ankle- and subtalar joints). The plantaris tendon runs

anteromedial to it. It is believed that in a healthy situation the plantaris tendon can move

freely in relation to the Achilles tendon. Adhesions between plantaris- and Achilles tendon

can be the results of an inflammatory response of the paratenon, which is located around

the Achilles- and plantaris tendons.

The plantaris muscle-tendon complex not only causes flexion but also inversion, whereas

the triceps surae is a flexor only. Adhesions between both tendons obstruct the opposite

forces of these two bi- and tri-articular muscle groups. Although the movement between the

two will be limited, traction onto the surrounding paratenon will take place with every step

Figure 4A-B. Endoscopic image of a patient with medial pain of his right Achilles tendon due to mid-portion Achilles tendinopathy. On Achilles tendoscopy the paratenon is released from the Achilles ten-don and in this image the plantaris tendon is identified. (A) The plantaris tendon is attached to the Achilles tendon. (B) With a trocar (in this case) the plantaris tendon is released from the Achilles tendon

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Figure 5A-D. The rationale of Achilles tendoscopy. (A) With a blunt trocar the paratenon is released from the Achilles tendon. (B) Thereby the nerves are destructed. (C) The plantaris tendon is cut at the level of complaints. (D) In the weeks postoperative, remnants of nerves obliterate and the proximal end of the plantaris tendon retracts

with a mean of 5,000 - 12,500 steps/ day in people with a low active to active lifestyle76,77.

Chronic painful tendons have been shown to exhibit new ingrowth of sensory nerve fibers

from the paratenon43,65. Repetitive traction onto this richly innervated area might contribute

to the medially located pain and stiffness during and after walking.

sUrGicAL treAtmeNt

Most surgical procedures aim at debridement or tenotomy of the tendon itself. In all these

procedures the paratenon is incised, released or removed as well. In open surgical debride-

ment of the tendon proper the paratenon has to be opened32,40,47,62, and during minimally

invasive tenotomy the paratenon is also addressed. It is therefore uncertain which part

of the procedure is responsible for a possible favourable outcome of such an approach.

Paratendinopathy and tendinopathy often co-exist. In some procedures only peritendinous

structures are addressed, such as in open or minimally invasive paratenectomy44,56 and

Achilles tendoscopy where the paratenon is released and the plantaris tendon cut to relieve

symptoms (Figure 5)51,69. These procedures render good results not in all, but in 75-100%

of patients. Aftertreatment most often is functional and recovery time, although not often

142

described, is 6 weeks to 6 months44,51,69,74. With surgery of the tendon proper, including

minimally invasive tenotomy, the tendon is temporarily weakened. Recovery time until sport

resumption therefore can be extensive and takes 3-18 months12,73,81.

How can the favourable results of addressing the paratenon only in patients with symptom-

atic Achilles tendinopathy be explained? Pain relief could be explained by destruction of the

sensory nerves running from the paratenon into the Achilles tendon proper in these chronic

patients: denervation of the Achilles tendon by releasing the paratenon may be the most

important part of all these procedures.

Positive results obtained from the more invasive conservative treatments may also be contrib-

utable to the destruction of nerve fibres. For example sclerosing injections with Polidocanol

and High Volume Image Guided Injections (HVIGI) aim at obliterating neovessels and the

accompanying nerve fibres6,13,29.

If pain can be relieved with denervation, extensive surgery of the tendon proper becomes

redundant.

coNcLUsioN

The goal of treatment of patients with chronic complaints of midportion Achilles tendinopa-

thy is to relieve pain. Many surgical procedures focus on the debridement of alterations in the

tendon proper. Since up to 34% of asymptomatic tendons show histopathological changes,

it is now believed that the tendon proper is not the cause of pain in the majority of patients

with symptomatic midportion Achilles tendinopathy. Chronic painful tendons show ingrowth

of sensory- and sympathetic nerves from the paratenon with release of nociceptive sub-

stances. Denervating the Achilles tendon by release of the paratenon, is sufficient to cause

pain relief in the majority of patients. This type of treatment has the additional advantage

that it is associated with a shorter recovery time when compared to treatment options that

address the tendon itself.

Ch

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143

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PArt iv retrocALcANeAL BUrsitis: DiAGNosis AND treAtmeNt

Chapter 9

Appearance of the weight- bearing lateral radiograph

in retrocalcaneal bursitis

MN van Sterkenburg

B Muller

M Maas

IN Sierevelt

CN van Dijk

Acta Orthop 2010; 81: 387-390

152

ABstrAct

Background and purposeA retrocalcaneal bursitis is caused by repetitive impingement of the bursa between the Achil-

les tendon and the posterosuperior calcaneus. The bursa is situated in the posteroinferior

corner of Kager’s triangle (retrocalcaneal recess), which is a radiolucency with sharp borders

on the lateral radiograph of the ankle. In case of inflammation, the fluid-filled bursa is less

radiolucent, making it difficult to delineate the retrocalcaneal recess. We assessed if the

radiographic appearance of the retrocalcaneal recess on plain digital (film-less) radiographs

could be used in the diagnosis of a retrocalcaneal bursitis.

MethodsObliteration of the retrocalcaneal recess (yes/no) on 74 digital weight- bearing lateral radio-

graphs of the ankle was independently assessed by 2 observers. Radiographs were of 24

patients (25 heels) with retrocalcaneal bursitis (confirmed on endoscopic calcaneoplasty); the

control group consisted of 50 patients (59 heels).

ResultsThe sensitivity of the test was was 83% for observer 1 and 79% for observer 2. Specificity

was 100% and 98% for observer 1 and 2. The interobserver reliability test calculated a

kappa-value of 0.86. For observer 1 intraobserver reliability was 0.96 and 0.92 for observer 2.

InterpretationThere is a typical appearance of the retrocalcaneal recess on digital weight-bearing lateral

radiographs of a retrocalcaneal bursitis.

Ch

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iNtroDUctioN

A symptomatic inflammation of the retrocalcaneal bursa is caused by repetitive impingement

of the bursa between the anterior aspect of the Achilles tendon and a bony posterosuperior

calcaneal prominence1,9,10.

Most publications focus on this protrusion, some describe a loss of radiolucency in Kager’s

triangle on lateral radiographs. Ultrasonography or MRI can be used to confirm the diagnosis.

Kager’s fat pad, also known as the pre-Achilles fat pad, occupies Kager’s triangle11. Normally

this fat pad, as seen on a weight-bearing lateral radiograph of the ankle, is a triangular

radio-lucency with sharp, gently curving borders4 (Figure 1).

The retrocalcaneal bursa is situated in the posteroinferior corner of the pad. In bursitis, the

normally sharply outlined radiolucent retrocalcaneal recess is obliterated (Figure 2).

There are few reports on the appearance of the retrocalcaneal recess on radiography and the

series are small5-7. These authors did not yet have the benefit of digital (film-less) examina-

tions with its advances of allowing images to be captured, viewed and reproduced digitally.

This offers several advantages, since contrast, brightness and magnification can be digitally

adjusted, and therefore a more sharp and detailed view is obtained.

We determined the reliability of the radiographical appearance of the retrocalcaneal

recess of Kager’s triangle in diagnosing a retrocalcaneal bursitis.

methoDs

24 patients (25 heels, 13 men) who had digital radiographs and had underwent endoscopic

calcaneoplasty for chronic retrocalcaneal bursitis from 2000-2008 were included (Figure 3). 1

patient underwent surgery on both ankles on different occasions. Mean age was 42 (15-73)

years. Patients with previous hindfoot surgery were excluded.

A control group matched for age and sex of 50 patients (59 heels, 30 men) with ankle prob-

lems not related to the hindfoot, was retrieved from our hospital’s archives from the same

period. From the 10 subjects with bilateral radiographs we randomly selected 1 heel, thus the

study comprised 74 heels (24 patients, 50 controls). Their mean age was 42 (15-72) years.

All heels had been examined with lateral weight-bearing radiographs in 20 degrees

endorotation, as is standard procedure in our hospital.

ObserversTo test interobserver reliability, all radiographs were independently evaluated by 2 experienced

observers: an orthopedic surgeon, and a radiologist. They rated the radiographs positive or

154

negative for the appearance of the retrocalcaneal recess (measurement 1). On a positive

radiograph the retrocalcaneal recess of Kager’s triangle was less radiolucent, meaning that it

was obliterated and had a whiter appearance; on a negative radiograph the retrocalcaneal

recess was radiolucent, meaning that it had a black appearance and its borders were sharp.

Both observers were blinded to the patient’s history. For intraobserver reliability testing, both

observers evaluated the radiographs 2 weeks later, which were now arranged in a different

order (measurement 2).

StatisticsDescriptive statistics on the patient’s demographics were performed. Sensitivity and specific-

ity were calculated to determine the validity of the test in predicting abnormality of the

retrocalcaneal recess of Kager’s triangle in retrocalcaneal bursitis.

Additionally, positive (PPV) and negative predictive values (NPV) were calculated.

For testing inter- and intraobserver reliability the Cohen’s kappa value was used. Kappa

values greater than 0.81 indicate high association. 95% confidence intervals were calculated

for each outcome.

SPSS for Windows version 15.0 was used to perform the analyses.

Figure 1. (A) Kager’s triangle with a normal appearance. (B) This triangular lucency with sharp, smooth-ly curving borders is indicated with the dotted line. (C) The arrowhead indicates the retrocalcaneal recess: the ‘bursal wedge’ of Kager’s fat pad, which normally forms a radiolucent corner posterosuperior to the calcaneus

Ch

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Figure 2. A patient with a chronic retrocalcaneal bursitis: the retrocalcaneal recess has disappeared because of the less radiolucent fluid in the distended retrocalcaneal bursa

Figure 3. (A) Clinical image, (B) Radiograph of a patient with a retrocalcaneal bursitis. The retrocalca-neal recess is obliterated by a chronic inflamed bursa (arrow). (C) Endoscopic view of a patient with a retrocalcaneal bursitis

156

resULts

We found a high sensitivity and specificity in both measurements for both observers as well

as high positive- and negative predictive values (PPV respectively NPV) (Table 1).

The interobserver reliability test for measurement 1 and 2 showed a high association

(Table 2). Intraobserver reliability also showed a high association in both observers (Table 3).

DiscUssioN

The terminology is confused when describing a retrocalcaneal bursitis, a syndrome of

combined bony and soft tissue pathology. Often, Haglund’s syndrome, Haglund’s disease,

Haglund’s deformity, pump-bump and retrocalcaneal bursitis are used interchangeably. To

avoid confusion, we chose to use the term ‘retrocalcaneal bursitis’, which is part of Haglund’s

syndrome and can be part of Haglund’s deformity. The bursal inflammation is the cause of

pain and the main reason for treatment.

We have found 2 studies on the appearance of the retrocalcaneal recess on conventional

radiographs. Pavlov et al. (1982)7 described 10 symptomatic heels and a control group of 78

heels. The goal of their study was to evaluate and describe all available clinical and radiologi-

cal findings in patients with Haglund’s syndrome. The appearance of the retrocalcaneal recess

was part of this evaluation. In 1 patient the retrocalcaneal recess was sharp, and in 9 it was

Table 1. Validity

Observer 1 2

Sensitivity (95%CI) 0.83 (0.58-0.96) 0.79 (0.54-0.93)

Specificity (95%CI) 1 (0.90-1) 0.98 (0.87-1)

PPV (95%CI) 1 (0.75-1) 0.94 (0.68-1)

NPV (95%CI) 0.93 (0.81-0.98) 0.92 (0.79-0.97)

Table 2. Interobserver reliability

Radiographs Kappa (95% CI)

Measurement 1 0.86 (0.71-1)

Measurement 2 0.87 (0.73-1)

Table 3. Intraobserver reliability

Radiographs Kappa (95% CI)

Observer 1 0.96 (0.87-1)

Observer 2 0.92 (0.80-1)

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ill-defined. Heneghan and Wallace (1985)6 described the appearance of the retrocalcaneal

recess in children.

6 heels were symptomatic, and the control group consisted of 24 heels. The purpose of

that study was to describe the osseous and soft tissue findings of retrocalcaneal bursitis and

to introduce roentgen criteria to substantiate the diagnosis. The retrocalcaneal recess was

one of these criteria. That study also found consistent loss of the sharp definition of the

retrocalcaneal recess in symptomatic patients.

What should be noted is that our lateral ankle radiographs are made weight-bearing and

in 20 degrees of endorotation, for parallel alignment of the lateral and medial malleolus and

to make sure the lateral and medial aspects of the talus overlap to be able to see the ankle

joint. This is not standard procedure everywhere, and if any, we are unaware of the effect on

the appearance of the retrocalcaneal recess.

When digital techniques are not available, conventional radiography may still suffice. It

is known that lowering the photon energy can be used to clarify details of soft tissues. The

results are essentially similar to increasing contrast in the evaluation of a digital radiograph,

which has been used in the past to assess patients with Achilles tendon problems2,3,8.

In conclusion, the radiographic appearance of the retrocalcaneal recess confirms the

clinical diagnosis of a retrocalcaneal bursitis. Further diagnostic evaluation is not necessary,

resulting in a higher cost-effectiveness and quicker treatment.

158

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Chapter 10

Endoscopic calcaneoplasty

MN van Sterkenburg

PAJ de Leeuw

CN van Dijk

Accepted in Minimally Invasive Foot & Ankle Surgery, editor Maffulli, 2010

Ch

apter 10

End

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161

iNtroDUctioN

In 1928, the Swedish orthopedic surgeon Patrick Haglund described a patient with a painful

hindfoot caused by a prominent posterosuperior aspect of the calcaneus in conjunction with

a sharp rigid heel counter8. The term Haglund’s disease, deformity and syndrome have been

used interchangeably, but have also been described as different entities by others.

Nowadays, the term ‘Haglund’s deformity’ is used to describe tenderness and pain on the

posterolateral aspect of the calcaneus. On physical examination, a bony prominence can

be palpated at this location. This entity is described by a variety of different names such as

‘pump-bump’5, ‘cucumber heel’6, ‘high-prow heels’31 and ‘winter heel’6.

There is more uncertainty on the definition of Haglund’s disease. It is described to be a

synonym for deformity or syndrome, but has also been referred to as an osteochondrosis of

the accessory navicular bone1,30,35. For this reason, it will not be considered in this chapter.

In Haglund’s syndrome, the retrocalcaneal bursa is inflamed with concomitant swelling. The

swelling is present on both sides of the Achilles tendon at the level of the posterosuperior

calcaneal prominence, sometimes in combination with insertional tendinopathy of the Achil-

les tendon. The syndrome is caused by repetitive impingement of the retrocalcaneal bursa

between the anterior aspect of the Achilles tendon and the enlarged posterosuperior aspect

of the calcaneus. It occurs most often at the end of the 2nd or the 3rd decade, mainly in

females, and is often bilateral. However, it may occur in both sexes and at any age.

In this chapter, the diagnosis and endoscopic treatment for patients with complaints of

a chronic retrocalcaneal bursitis is described, which can be part of Haglund’s deformity and

Haglund’s syndrome.

DiAGNosis

Patients typically describe the onset of pain when starting to walk after a period of rest.

The distinction between Haglund’s deformity, Haglund’s syndrome, and other pathologic

conditions of the posterior aspect of the heel, most importantly Achilles tendinopathy,

should be made.

Insertional tendinopathy is defined as a tendinopathy of the tendon at its insertion. The pain

is most frequently located in the midline at the insertion into the calcaneus. Co-existence

with retrocalcaneal bursitis is known.

In Haglund’s deformity, a bony prominence can be seen at the posterosuperolateral aspect of

the heel, which is painful on palpation. The superficial bursa may be swollen, and the overly-

ing skin can be thickened and dyschromic. A retrocalcaneal bursitis occasionally develops as

a result of this deformity.

In Haglund’s syndrome, on physical examination swelling can be seen on both sides of the

tendon at the level of the posterosuperior calcaneal prominence, and pain can be reproduced

162

by palpation of the lateral and medial side of the Achilles tendon at this level. With dorsi-

flexion of the ankle, the anterior part of the tendon impinges against the posterosuperior

rim of the calcaneus, leading to retrocalcaneal bursitis. A hindfoot varus and a pes cavus

are both predisposing factors for heel pain. In the cavus foot, the calcaneus is not only in

varus malalignment, but it is also more vertical, which results in a more prominent projection

posteriorly7.

mANAGemeNt

Multiple options have been described to manage chronic retrocalcaneal bursitis, including

avoidance of tight shoe heel counters, cast immobilization, NSAIDs, activity modification,

padding, shock wave treatment, physical therapy and a single injection of corticosteroids

into the retrocalcaneal space. If conservative management fails, there are essentially two

distinct operative methods, and one endoscopic surgical technique. The open operative

alternatives include resection of the posterosuperior part of the calcaneus or a calcaneal

wedge osteotomy. Complications include skin breakdown, tenderness in the region of the

operative scar, esthetically non-appealing operative scars and altered sensation around the

heel2,9,15,19,25. More serious complications include Achilles tendon avulsions and calcaneal

(stress) fractures14,15,19. Recurrent persistent pain secondary to an inadequate amount of

bone resected, and stiffness of the Achilles tendon resulting in decreased dorsiflexion have

also been reported22. Wound healing problems have been described in 30% of patients

treated with open procedures29.

eNDoscoPic treAtmeNt

Endoscopic treatment offers advantages that are related to any minimal invasive surgi-

cal procedure, such as a low morbidity, excellent scar healing, functional aftertreatment,

Figure 1. (A) A patient with Haglund’s syndrome in the right hindfoot. (B) The typical swelling (S) on both sides of the Achilles tendon (AT) at the level of the posterosuperior calcaneal prominence is indi-cated

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A B

C D

Figure 2. (A) Schematic lateral view of a hindfoot showing Kager’s triangle (black). (B) Plain conven-tional lateral standing radiograph of an ankle with a normal aspect of the bony and soft tissues in the hindfoot. Kager’s triangle is indicated (dotted line). The arrow points at the retrocalcaneal recess. (C) Kager’s triangle is schematically drawn (black). Indicated in red is the fluid-filled retrocalcaneal bursa. (D) Lateral standing radiograph of a patient’s right ankle showing hypertrophy of the posterosuperior aspect of the calcaneus with infiltration of the retrocalcaneal recess of Kager’s triangle by the fluid-filled retrocalcaneal bursa

short recovery time and a shorter time to sport resumption as compared to open surgical

approaches. Here we describe the technique of endoscopic calcaneoplasty, and compare

the results of this minimal invasive technique34 with those reported for the open surgical

techniques.

IndicationPatient complaints include pain at rest, when standing, walking (uphill), running and walking

on hard surfaces. Conventional lateral radiographs show hypertrophy of the posterosuperior

164 Figure 3. The patient is placed in prone position (A). The affected right leg is placed on a bolster and right over the end of the table (B). The other foot is positioned in a way that the surgeon has sufficient working area (C)

Figure 4. (A) Schematic drawing of lateral view of the foot. The ankle is placed in plantigrade position. A line is drawn through the tip of the fibula parallel to the sole of the foot. The incision for the lateral portal in conventional posterior arthroscopy is placed directly above this line; the center of the incision in pa-tients undergoing endoscopic calcaneoplasty is placed 1.5-2.5 cm below this line (red). (B) Preoperatively this can be verified by drawing these same lines on a lateral standing radiograph of the foot. (C) Location of lateral and medial (D) portal as indicated by the probe (red line)

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aspect of the calcaneus and deep retrocalcaneal bursitis, identified by diminished radiolu-

cency of the retrocalcaneal recess and the lower portion of Kager’s triangle (Figure 2).

If conservative treatment fails, we undertake endoscopic surgery.

Surgical techniqueSurgery is performed with the patient in prone position under general or regional anesthesia.

The involved leg is marked with an arrow by the patient, to avoid wrong side surgery. The

feet are positioned just over the edge of the operation table. The involved leg is slightly

elevated by placing a bolster under the lower leg (Figure 3).

The position of the foot is in plantarflexion through gravity. Prior to surgery important ana-

tomical structures are marked. These include the medial and lateral border of the Achilles

tendon and the calcaneus (Figure 4).

The lateral portal is made first, just lateral of the Achilles tendon at the level of the superior

aspect of the calcaneus. This portal is produced as a small vertical incision through the skin

only. The retrocalcaneal space is penetrated with a blunt trocar. A 4.5 mm arthroscopic shaft

with an inclination angle of 30o is introduced (Figure 5).

Irrigation is performed by gravity flow. A 70o arthroscope can also be used but is seldom

necessary. Under direct vision, a spinal needle is introduced just medial to the Achilles ten-

don, again at the level of the superior aspect of the calcaneus, to locate the medial portal

(Figure 6).

After having prepared the medial portal by a vertical stab incision, a 5.5 mm bonecutter

shaver (Dyonics Bonecutter, Smith & Nephew, Andover, USA) is introduced and visualized

by the arthroscope. The inflamed retrocalcaneal bursa is removed first (Figure 7) to provide

a better view. Now the superior surface of the calcaneus is visualized and its fibrous layer

Figure 5. (A) incision for lateral portal in a left ankle. (B) Penetration of retrocalcaneal space with blunt trocar followed by blunt dissection. (C) Introduction of arthroscope with 30 o inclination angle

166 Figure 6. (A) Introduction of spinal needle (left ankle) under direct vision (B) for placement of medial portal

Figure 7. Endoscopic calcaneoplasty of the right hindfoot of a 38-year-old female patient with Haglund’s syndrome. (A) The retrocalcaneal recess. AT= Achilles tendon; INF= inflamed retrocalcaneal bursa; CA= calcaneus. (B) Retrocalcaneal bursa is removed with bonecutter shaver. BS= bonecutter shaver

Figure 8. (A) Removal of bone at the posteromedial border of the calcaneus with arthroscope in the lateral portal. (B) Removal of bone at the lateral border of the calcaneus after change of portals. AT= Achilles tendon; BS= bonecutter shaver; PM= posteromedial border of calcaneus; LB= posterolateral border of calcaneus; CA= calcaneus

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and periosteum are stripped off. During resection of the bursa and the fibrous layer and

periosteum of the superior aspect of the calcaneus, the full radius resector is facing the bone

to avoid damage to the Achilles tendon.

When the foot is brought into full dorsiflexion, impingement between the posterosuperior

calcaneal edge and the Achilles tendon can be perceived. The foot is subsequently brought

into plantarflexion and now the posterosuperior calcaneal rim is removed. This bone is quite

soft and can be removed by the aggressive synovial full radius resector or bone cutter. A burr

is not needed at this point. The portals are used interchangeably for both the arthroscope

and the resector, so as to remove the entire bony prominence. It is important to remove a

sufficient amount of bone at the posteromedial and lateral corner (Figure 8). These edges

have to be rounded off by moving the synovial resector beyond the posterior edge onto the

lateral respectively medial wall of the calcaneus.

The Achilles tendon is protected throughout the entire procedure by keeping the closed

end of the resector against the tendon. With the foot in full plantarflexion, the insertion of

the Achilles tendon can be visualized.

The bonecutter is placed on the insertion against the calcaneus to smoothen this part of the

calcaneus. Finally, the resector is introduced to clean up loose debris and to smooth pos-

sible rough edges. In the first several patients, fluoroscopic control can be used to ascertain

whether sufficient bone has been resected. With some experience, this will no longer be

necessary. Figure 9 shows an endoscopic view of the end result.

To prevent sinus formation, at the end of the procedure the skin incisions are closed with

3.0 Ethilon sutures. The incisions and surrounding skin are injected with 10 ml of a 0.5%

bupivacain/morphine solution. A sterile compressive dressing is applied.

Post-operative managementPostoperatively, the patient is allowed weight -bearing as tolerated and is instructed to elevate

the foot when not walking. The dressing is removed 3 days postoperatively, after which the

patient is allowed to shower. Patients are encouraged to perform active range of motion

exercises for at least 3 times a day for 10 minutes each. The patient is allowed to return

to wearing regular shoes as soon as tolerated. The sutures are removed after two weeks.

A conventional lateral radiograph is made to ensure that sufficient bone has been excised

(Figure 10). With satisfaction of the surgeon and patient, no further outpatient department

contact is necessary. Patients with limited range of motion are directed to a physiotherapist.

Patient outcomeBetween 1995 and 2000 in the Academic Medical Center in Amsterdam we performed 39

procedures in 36 patients28. The average age was 35 years (range 16-50). Patients had a

168

Figure 9. Result at the end of procedure. CA= calcaneus, BS= bonecutter shaver, AT= Achilles tendon

Figure 10. (A) Preoperative X-ray, with retrocalcaneal bursitis and prominence of the posterosuperior part of the calcaneus (arrow). (B) postoperative X-ray. The posterosuperior part of the calcaneus is suf-ficiently excised (arrow)

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painful swelling of the soft tissue of the posterior heel, medial and lateral of the Achilles

tendon on physical examination, without pain on palpation of the tendon itself. Conservative

management for at least 6 months did not relieve symptoms. The conventional lateral radio-

graph showed a superior calcaneal angle (subtended by lines drawn from the bursal projec-

tion to the posterior calcaneal tuberosity and from the medial calcaneal tuberosity to the

anterior calcaneal tuberosity) of more than 75°. An angle larger than 75° has been deemed

pathologic6,31. The mean follow up after endoscopic calcaneoplasty was 4.5 years (range

2 - 7.5). There were no surgical complications except from one 1 patient who experienced

an area of hypoesthesia over the heel pad. Postoperatively there were no infections, tender

or esthetically non-appealing scars and all patients were content with their small incisions.

Except for two patients, all patients improved. The Ogilvie-Harris score23 was rated fair by 4

patients, 6 rated good and 24 had excellent results. Work and sport resumption took place

at an average of 5 weeks (range 10 days-6 months) and 11 weeks (range 6 weeks-6 months)

respectively28,34.

DiscUssioN

Conservative management for retrocalcaneal bursitis includes a single cortisone injection in

the retrocalcaneal bursa21,22,32. Repeated injections are not advised since these can weaken

the tendon with the potential danger of rupture.

The aim of surgery for retrocalcaneal bursitis, after failure of the conservative treatment,

is preventing impingement between the Achilles tendon and the calcaneus. This can be

accomplished by means of removing the inflamed retrocalcaneal bursa followed by either

resection of the posterosuperior calcaneal rim or by a closing wedge osteotomy. Postero-

superior calcaneal resection can be performed through a posterolateral or posteromedial

incision or via a combination of both2,13,25.

A widely used technique, especially in North America, is the midline-posterior skin incision

combined with a central tendon splitting approach for debridement, retrocalcaneal bursec-

tomy, and removal of the calcaneal bursal projection as necessary18. Another approach is

the Cincinnati-type incision, a transverse skin incision at the level of the insertion of the

Achilles tendon. With this technique, a wide exposure of the insertion of the Achilles tendon

is possible, to debride the peritendinous and tendon tissue and if necessary bursectomy. The

transverse skin incision at the level of the Achilles insertion also allows osteotomy of the

posterosuperior corner of the calcaneus4, and, being in the direction of the skin creases, it

has a lesser potential for healing problems than the longitudinal approaches.

Endoscopic calcaneoplasty offers a good, minimally invasive alternative to open surgery.

Surgeons familiar with the endoscopic approach tend to favor this procedure, because of its

better visualization as compared to the open procedure. Due to inappropriate visualization

of the Achilles tendon during the open procedure, weakening or even rupture of this tendon

170

has been reported14,19. Full recovery time after the open resection can take as long as 2

years. Our patient series shows a high percentage of good to excellent results based on the

Ogilvie- Harris score.

Our results are comparable with other recently published reports on endoscopic treat-

ment.

Jerosh and co-workers published a prospective study in which they described the results of

endoscopic calcaneoplasty in 81 patients with an average follow-up of 35.3 months (range

12 to 72). Using the Ogilvie-Harris score, 41 patients presented excellent results, 34 pre-

sented good results, 3 had fair, and 3 patients showed poor results. These 3 patients showed

an ossified area of the Achilles tendon insertion, and were revised in an open procedure. Only

one patient experienced a superficial inflammation of the skin was found10,11. Ortmann and

co-workers operated on 30 patients (32 heels) with retrocalcaneal bursitis with the endo-

scopic technique. The means follow-up was 35 months, and the AOFAS score averaged 62

preoperatively and 97 postoperatively. There were 26 excellent results, three good results and

one poor result. One patient ruptured an Achilles tendon, one had residual pain and swelling

that required reoperation through an open procedure. There were no other complications.

Patients returned to work after on average of 8 weeks, and all athletes resumed their sport-

ing activities in an average of 12 weeks24.

Morag and co-workers treated 4 patients with endoscopic calcaneoplasty, and after an

average follow-up of 2 years (range 1 to 3.5 years), no complications, pain, disability, or

range of motion deficits were reported20.

The advantages of the endoscopic over the open procedure are the small incisions, avoiding

complications such a wound dehiscence, painful and/or ugly scars and nerve entrapment

within the scar, as described for the open procedure9. He found a considerable amount

of residual complaints in 32 clinically and radiographically examined patients treated by

surgical resection of the posterosuperior calcaneal prominence for Haglund’s syndrome at a

mean follow-up of 18.6 years (range 2-41). 14 of these 32 patients had soft tissue problems

including excessive scar formation and persistent swelling. In 8 patients not enough bone

was excised and 2 had new bone formation, both resulting in persistent painful swelling. The

function of the Achilles tendon was disturbed in 8 patients9.

There is no consensus regarding the ideal open surgical approach: medial, lateral, or

both2,12,25. Jones and James performed 10 partial calcaneal osteotomies for retrocalcaneal

bursitis, followed by a short leg walking cast for 8 weeks, progressively increasing weight-

bearing. Rehabilitation consisted of wearing an elevated heel of 1 inch until the foot came

easily to the neutral position. All patients were back to their desired level of activity within 6

months12. Angermann operated on 40 heels for the same indication using the posterolateral

approach in 32 patients. Postoperatively 29 patients were allowed immediate weight-

bearing. Complications consisted of one superficial heel infection, one haematoma and two

patients with delayed skin healing. At an average follow-up of 6 years (range 1-12) 50%

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of the patients were cured, 20% improved, 20% remained unchanged and in 10% the

pre-operative symptoms worsened2. The rate of poor results in this study corresponds to the

results of Taylor, who reported 36% poor results after the same type of surgery33. Pauker

and co-workers operated on 28 heels in 22 patients with Haglund’s syndrome. 18 heels

were approached laterally, and 10 medially, depending on the direction of the prominent

bone. All patients received a short leg walking cast for 4 weeks followed by mobilization

exercises for aftertreatment. At a mean follow up of 13 years in 19 patients (range 3-20), 15

had good results, 2 fair and 2 poor. No difference in outcome between the two approaches

was reported. The authors advocate using one incision, as many patients have complaints of

tenderness over the operative scar up to one year postoperatively which might be exagger-

ated by a more extensive approach25.

Schepsis and co-workers used the medial approach in 24 patients with retrocalcaneal

bursitis: 6 (25%) had a fair result requiring re-operation. In 49 heels (36 patients) operated

through a lateral approach with a mean follow-up of 4.7 years (range 1 to 11 years), early

complications were reported in 4 cases (3 haematomas and a superficial infection), and

late complications in 3 cases resulting in revision surgery. 7 patients noted some improve-

ment, 1 patient described no change and 7 patients reported worsening of their symptoms

after surgery27. Brunner and co-workers performed calcaneal osteotomies on 39 heels (36

patients), and reported at an average follow-up of 51 months, an average improvement of

the AOFAS score of 32 points as compared to the mean pre-operative score. Recovery time

ranged from 6 months up to 2 years. 6 of the 36 patients reported persisting posterior heel

pain after surgery3.

There are two comparative studies in which both endoscopic and open procedures were

performed. Leitze and co-workers compared the endoscopic approach (n=30, 22 months

follow-up) with the open surgical technique (n=17, 42 months follow-up). The endoscopic

approach revealed 19 excellent, 5 good, 3 fair and 3 poor results, which was numerically

but not significantly better than the open surgical procedure. Recovery time was identical,

but operation time, the amount of complications and scar tissue formation favoured the

endoscopic approach16. In a recent study by Lohrer and co-workers, a comparison was made

between the endoscopic and open resection for Haglund’s syndrome. In this anatomic study,

9 cadaver feet were operated by means of open surgery and 6 were operated through

endoscopic calcaneoplasty. After the procedure the ankles were dissected to determine the

amount of damage following the surgery. Comparable amounts of damage were found for

the sural nerve, the plantaris tendon and the medial column of the Achilles tendon17. Since

this was an anatomic study, no data could be gathered regarding recovery time and scar

healing, which seem to be the advantageous points of the endoscopic procedure. Also,

cadaveric ankles could have been stiffer as compared to patients, which made the endo-

scopic approach more difficult to perform.

172

Overall, looking at the available results of open surgery, studies reported 61-83% good

results and 17-36% complications or poor results requiring re-operation3,12,16,25,26,33.

Endoscopic surgery leads up to an estimated rate of 83-93% good results, and 0.6- 5%

complications or poor results requiring re-operation9,11,24,28.

coNcLUsioN

In summary, whether the operation is performed by endoscopic or open surgery, enough

bone has to be removed to prevent impingement between the calcaneus and Achilles tendon.

The endoscopic calcaneoplasty has demonstrated to show several advantages including low

morbidity, functional aftertreatment, outpatient treatment, excellent scar healing, a short

recovery time and quick sport resumption as compared to the results for the open technique.

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1. Alm A, Lamke LO, Liljedahl SO. Surgical

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tendons. Injury 1975; 7(1): 14-19.

2. Angermann P. Chronic retrocalcaneal bur-

sitis treated by resection of the calcaneus.

Foot Ankle 1990; 10(5): 285-287.

3. Brunner J, Anderson J, O’Malley M, Bohne

W, Deland J, Kennedy J. Physician and

patient based outcomes following surgical

resection of Haglund’s deformity. Acta

Orthop Belg 2005; 71(6): 718-723.

4. Carmont MR, Maffulli N. Management of

insertional Achilles tendinopathy through

a Cincinnati incision. BMC Musculoskelet

Disord 2007; 8: 82.

5. Dickinson PH, Coutts MB, Woodward EP,

Handler D. Tendo Achillis bursitis. Report

of twenty-one cases. J Bone Joint Surg Am

1966; 48(1): 77-81.

6. Fowler A. Abnormalities of the calcaneus

as a cause of painful heel: its diagnosis and

operative treatment. Br J Surg 1945; 32: 494-

498.

7. Fuglsang F, Torup D. Bursitis retrocalcanearis.

Acta Orthop Scand 1961; 30: 315-323.

8. Haglund P. Beitrag zur Klinik der Achil-

lessehne. Zeitschr Orthop Chir 1928; 49:

49-58.

9. Huber HM, Waldis M. [The Haglund

exostosis--a surgical indication and a minor

intervention?]. Z Orthop Ihre Grenzgeb

1989; 127(3): 286-290.





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12. Jones DC, James SL. Partial calcaneal ostec-

tomy for retrocalcaneal bursitis. Am J Sports

Med 1984; 12(1): 72-73.

13. Kolodziej P, Glisson RR, Nunley JA. Risk

of avulsion of the Achilles tendon after

partial excision for treatment of insertional

tendonitis and Haglund’s deformity: a

biomechanical study. Foot Ankle Int 1999;

20(7): 433-437.



8(3): 601-623.

15. Leach RE, DiIorio E, Harney RA. Pathologic

hindfoot conditions in the athlete. Clin

Orthop Relat Res 1983; (177): 116-121.

16. Leitze Z, Sella EJ, Aversa JM. Endoscopic

decompression of the retrocalcaneal space.


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17. Lohrer H, Nauck T, Dorn NV, Konerding MA.

Comparison of endoscopic and open resec-

tion for Haglund tuberosity in a cadaver

study. Foot Ankle Int 2006; 27(6): 445-450.

18. McGarvey WC, Palumbo RC, Baxter DE,

Leibman BD. Insertional Achilles tendinosis:

surgical treatment through a central tendon

splitting approach. Foot Ankle Int 2002;

23(1): 19-25.

19. Miller AE, Vogel TA. Haglund’s deformity

and the Keck and Kelly osteotomy: a ret-

rospective analysis. J Foot Surg 1989; 28(1):

23-29.

20. Morag G, Maman E, Arbel R. Endoscopic

treatment of hindfoot pathology. Arthros-

copy 2003; 19(2): E13.

21. Myerson MS, McGarvey W. Disorders of the

Achilles tendon insertion and Achilles tendi-

nitis. Instr Course Lect 1999; 48: 211-218.

22. Nesse E, Finsen V. Poor results after resection

for Haglund’s heel. Analysis of 35 heels in

23 patients after 3 years. Acta Orthop Scand

1994; 65(1): 107-109.

23. Ogilvie-Harris DJ, Mahomed N, Demaziere A.

Anterior impingement of the ankle treated

by arthroscopic removal of bony spurs. J

Bone Joint Surg Br 1993; 75(3): 437-440.

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24. Ortmann FW, McBryde AM. Endoscopic

bony and soft-tissue decompression of

the retrocalcaneal space for the treatment

of Haglund deformity and retrocalcaneal

bursitis. Foot Ankle Int 2007; 28(2): 149-153.

25. Pauker M, Katz K, Yosipovitch Z. Calcaneal

ostectomy for Haglund disease. J Foot Surg

1992; 31(6): 588-589.

26. Schepsis AA, Wagner C, Leach RE. Surgical

management of Achilles tendon overuse

injuries. A long-term follow-up study. Am J

Sports Med 1994; 22(5): 611-619.

27. Schneider W, Niehus W, Knahr K. Haglund’s

syndrome: disappointing results following

surgery -- a clinical and radiographic analy-

sis. Foot Ankle Int 2000; 21(1): 26-30.

28. Scholten PE, van Dijk CN. Endoscopic

calcaneoplasty. Foot Ankle Clin 2006; 11(2):

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24(3): 252-267.

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Haglund’s Syndrome. J Foot Ankle Surg

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Am 1994; 25(1): 41-46.

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Chapter 11

Optimization of portal placement for endoscopic calcaneoplasty

MN van Sterkenburg

M Groot

IN Sierevelt

GMMJ Kerkhoffs

CN van Dijk

Arthroscopy 2011; 27: 1110-1117

176

ABstrAct

Purpose The purpose of our study was to determine an anatomical landmark to help locate portals in

endoscopic calcaneoplasty (EC).

MethodsThe DOPP (Device for Optimal Portal Placement) was developed to measure the distance

from the distal fibula tip to the calcaneus (DFC) in 28 volunteers to determine the location of

the posterosuperior calcaneal border in relation to this line.

ResultsThe DOPP demonstrated an inter-observer reliability of 0.99 (95%CI 0.97-0.99). We found

that in patients with flat feet, portals should be placed at a mean of 15 mm (SD 4.5) distal to

the tip of the fibula, in normal feet at 20 mm (SD 4.8) and in cavus feet at a mean of 22 mm

(SD 5.4). The difference of the DFC within the 3 different foot type groups was significant

(p<0.05).

ConclusionsThe DOPP demonstrated to be highly reliable in measuring the DFC (ICC= 0.99). A numeric

distance scale for use in all different foot morphologies could not be constructed. There is a

direct relation between portal location and foot morphology (p<0.05), as in flat feet portal

location is significantly more proximal (15 mm) to the tip of the fibula when compared to

cavus feet (22 mm).

Clinical relevanceThese results may help with portal placement in endoscopic calcaneoplasty for all different

foot morphologies.

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iNtroDUctioN

Endoscopic calcaneoplasty (EC) has demonstrated to be an effective surgical procedure

for treatment of patients with complaints of a retrocalcaneal bursitis not responding to

conservative treatment5,6,14,19. Two portals are used, just lateral and medial to the Achilles

tendon, at the level of the posterosuperior tuberosity of the calcaneus (Figure 1). During the

procedure, the inflamed retrocalcaneal bursal tissue and posterosuperior tuberosity of the

calcaneus are resected. However, due to the local anatomy, bulky subcutaneous tissue and

swelling of the retrocalcaneal bursal tissue, palpation of the posterosuperior calcaneal rim

is difficult and portals can easily be placed too far proximal. This will result in a suboptimal

procedure. Fluoroscopy is sometimes used to make portals, but can be time-consuming and

the surgeon has to depend on availability and personnel. Additionally, retrocalcaneal bursitis

often occurs in young patients in whom especially radiation has to be limited to a minimum.

For this reason there is need for standardization of these portals. Portals in the area that have

been standardised are those for hindfoot endoscopy18.

In the standard 2-portal hindfoot technique, the distal tip of the fibula is used as an ana-

tomical landmark for placement of the posteromedial and -lateral portal16-18. A probe is

hooked under the tip and is held parallel to the foot sole which in turn is placed in a 90

degree position with the lower leg. A (imaginary) line is drawn from the tip to the Achilles

tendon and the portals are made just above this line (Figure 2). The aim of this study was to

determine the optimal location for the portals in EC in relation to this line and to determine

if this distance is reproducible in all individuals.

Figure 1. (A) Medial and lateral portal for endoscopic calcaneoplasty (red marks). Portals are placed at the posterosuperior calcaneal tuberosity. (B) Arthroscope is placed in the lateral- and a bonecutter shaver in the medial portal

178

The hypotheses were that the DOPP is a valid tool for standardizing portal placement, and

that using the distance from the distal tip of the fibula to the posterosuperior calcaneus (DFC)

on a radiograph would help us determine the ultimate position of portals, and provide us

with a numeric distance- scale to be used in all different foot morphologies.

methoDs

PopulationThis study was approved by our local Medical Ethical Committee.

It was decided to use healthy volunteers, as the goal of the procedure is to correct the

posterosuperior calcaneus to a normal situation with some overcorrection. Portals should

not be placed above a possible posterosuperior calcaneal prominence, as the shaver may

consequently not be able to reach the level of insertion.

28 volunteers with a mean age of 25 (SD 3.7) without a history of foot surgery or

trauma were recruited. Informed consent was signed, patient history was taken and physical

examination was performed to assess foot morphology. Of each volunteer one foot was

used for measurements and analysis2. Age, weight, length and Body Mass Index (BMI) were

recorded. Of all volunteers 3 lateral radiographs were made.

Foot morphologyWe considered foot morphology important since as the calcaneus tilts the DFC probably

increases with cavus- and decreases with flat feet (Figure 3). It was decided to group mor-

phology into three generally used types: cavus, normal, and flat feet.

Figure 2. (A) The tip of the fibula, used as a landmark in the standard 2-portal hindfoot procedure. The lateral incision in standard posterior arthroscopy is made just lateral to the Achilles tendon. The portal for endoscopic calcaneoplasty is located at the level of the posterosuperior calcaneal tuberosity (white mark in B)

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179Figure 3. The DFC is larger in cavus feet (A) as compared to flat feet (B)

Figure 4. (A) The TMT1- angle measures the alignment of the forefoot with respect to the hindfoot, which is useful for interpretation of cavus and planus deformities. The intersection of the talar and the first metatarsal longitudinal axes creates this angle. Normal is 0°, whereas angles are increasingly nega-tive for cavus deformities (forefoot plantar flexion on the hindfoot) and increasingly positive for flat foot malformations (forefoot dorsiflexion on the hindfoot)1,3,7,9,10,15,20. The TMT1-angle is the intersection of the talar and the first metatarsal longitudinal axes. (B) The CI-angle is measured by a line passing parallel to the floor and a second line passing along the inferior border of the calcaneus (Figure 4B). A normal angle is 30°, in cavus feet it is more than 30°, and in flatfeet it is decreased 1,9,13,15

Physical examination as well as radiography was used to determine foot morphology. A foot

was defined as ‘flat’ when there was flattening of the medial longitudinal arch in weight-

bearing and apparent bowing of the Achilles tendon to medial (Helbing sign) as viewed from

posterior. A foot was defined as cavus when there was hindfoot varus and an increase in

height of the medial longitudinal arch of the foot that did not flatten on weight-bearing.

Talo 1st metatarsal (TMT1) - and calcaneal inclination (CI) angles11,12 as measured on a

standard lateral weight-bearing radiograph of the foot were used (Figure 4).

The DOPP, ‘Device for Optimal Portal Placement’It was aimed to measure the DFC on a lateral radiograph. This appeared impracticable since

overlying structures make the tip of the fibula difficult to identify. Also, when measuring the

DFC per-operatively on a patients foot, there is soft tissue interposition between probe and

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fibula. Therefore we constructed a device prior to study initiation with which a metal probe

can be hooked underneath the tip of the fibula, hereby mimicking the setting in standard

2-portal hindfoot endoscopy (Figure 5A).

Radiographs with the DOPP were made in a sitting position with the ankle in 90° (Figure 5B).

We chose this position to reproduce the conditions of the surgical procedure as accurate

as possible. The surgeon positions the ankle in 90° when creating the portals in standard

2-portal hindfoot endoscopy. We consider the force used by the surgeon best comparable

to the axial force sitting-down. The device was handled by 1 observer throughout the study

and repositioned with each radiograph.

RadiographsAll radiographs were made by a radiology technician. Per volunteer 1 standard lateral

weight-bearing radiograph with the foot in 20 degrees endorotation and 2 radiographs with

the DOPP (alternative radiographs) were made. Radiographs with the DOPP were made in a

neutral position to mimic the surgical setting. Next to measuring the DFC, the 2 radiographs

with the DOPP were also used to assess intra-observer reliability of placement of the DOPP.

All measurements were performed digitally using PACS (Picture Archiving and Communica-

tion System) Viewer by Agfa Health Care, Mortsel, Belgium.

Measurement of the DFC on radiographs was performed according to the methods explained

in figure 6. The acceptable variation of the DFC between two measurements per volunteer

was set to a maximum of 5 mm. This is the diameter of the bonecutter shaver used, chosen

as the radius in which the shaver can be moved without having to lengthen or change portal

location. We use this shaver to reduce the tuberosity in EC. If variation remained within a

limit of 5 mm, the retrocalcaneal space would still be accessible for the surgeon.

Figure 5. (A) Portal placement in standard posterior arthroscopy, using the distal tip of the fibula as a landmark. (B) Mimicking this surgical setting with the DOPP

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Figure 6. Digitally measured distance between the posterosuperior part of the calcaneus and the distal tip of the fibula (DFC, red arrow). Line A: foot sole; Line B: probe of the DOPP hooked under the tip of the fibula (which seems separate from the bone due to soft tissue interposition); Line C: continuation of a line through the vertical aspect of the posterior calcaneal tuberosity; Line D: prolongation of a hori-zontal line from the anterior to the posterior aspect of the calcaneal tuberosity; Line E: helpline parallel to line B (and A) through the junction of lines C and D

For all measurements intra- and interobserver reliability were calculated.

StatisticsResults were analyzed with SPSS (Statistical Package for the Social Sciences) 15.0 for Win-

dows. Volunteer characteristics are described as means and standard deviations or propor-

tions.

For intra- and interobserver reliability for the measurements of the CI- and TMT1- angles,

Intra Class Coefficients (ICC) with 95% confidence intervals (CI) were calculated; an ICC

of 0 - 0.2 indicates a poor reliability, 0.21 - 0.4 is fair, 0.41 – 0.6 is moderate, 0.61 – 0.8 is

substantial, and values between 0.81- 1.0 indicate high reliability8.

Intra-observer reliability for handling the DOPP was tested by calculating ICCs with a 95%

CI. To illustrate the variation for repeated measurements, we presented a Bland and Altmann

plot. This shows the limits of agreement and the 95% confidence interval with an acceptable

variation of 0 ± 5 mm.

182

The clinical validity of the DOPP was assessed through determination of the differences in dis-

tance measured on radiographs between the three foot types by means of an ANOVA-test,

and if necessary, an additional post hoc Bonferroni multiple comparisons test was applied.

Pearson correlation coefficients were calculated to assess association between DFC and

TMT1- and CI- angles, length and shoe size.

Spearman r correlation coefficients were calculated between the DFC and the categorized

variable (foot type according to physical examination).

Pearson- and Spearman correlation coefficients were interpreted as 0.0-0.2 being no; 0.2-

0.4 low; 0.4-0.7 moderate; 0.7-0.9 high; and above 0.9 very high4. A p-value < 0.05 was

considered statistically significant.

Figure 7. Bland and Altmann plot

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resULts

Demographic StatisticsDemographics of the volunteers are shown in Table 1. Twenty-four (85.7%) participants

actively participated in different sports. A ‘too many toes-sign’ was observed in 7 volunteers

(25%).

According to physical examination, we included 10 volunteers with normal feet (a normal

arch), 11 with flat feet (flat arch) and 7 volunteers with cavus feet (high arch).

Table 1. Demographics of the subjects, in means and standard deviations (in brackets)

Volunteers (n=28)

Age (years) 24.5 (±3.7)

Male/Female 8/20

Weight (kg) 69.3 (±13.3)

Length (m) 1.75 (±0.1)

BMI (in kg/m²) 22.5 (±3.5)

Left/right foot 15/13

Talo 1st metatarsal (TMT1) and calcaneal inclination (CI) angleThe forefoot of the first five consecutive volunteers was not properly visible on radiographs

because of technical difficulties, making it impossible to measure the TMT1-angle. We did

not make an additional radiograph to prevent them from exposition to more radiation than

agreed upon with the Medical Ethical Committee. The mean TMT1- angle was 0.1o (SD 9.8).

According to the classification described earlier, 9 had a flat arch, 6 had a normal arch and 8

volunteers had a high arch. Intra-observer reliability for the TMT1-angle showed ICC values

of 0.98 for both observers. Inter-observer reliability for the TMT1-angle was high with an ICC

of 0.91 (Figure 7).

The mean CI- angle was 21o (SD 6.1). According to the classification, 13 volunteers had a

flat arch, 12 a normal arch, and 3 a high arch. Intra-observer reliability for the CI-angle was

0.99 for both observers. The inter-observer reliability showed an ICC-value of 0.98.

No significant correlation was found between BMI, and TMT1- and CI- angle (p>0.1).

The DOPPThe intra-observer reliability for handling the DOPP, demonstrated an ICC of 0.96. The inter-

observer reliability for radiographic measurements of the DFC showed an ICC of 0.99 (95%

CI 0.97-0.99). Figure 7 shows the variation for repeated measurements. The red dotted lines

indicate the acceptable variation of 0 ±5 mm. 95% of our measurements lie within 3.4 and

-3.7 mm. This is within limits. In one volunteer the difference in DFC between two measure-

ments was more than 5 mm due to an error positioning the DOPP for the first radiograph.

184

Correlation between the radiological measurements and physical examination showed that

the TMT1-angle had the best correlation (Table 2).

DFC in different foot morphologiesCorrelation between the DFC and different variables are shown in Table 3.

The Spearman r correlation analysis revealed moderate correlations (r = 0.54 and 0.60, p

< 0.05) between foot morphology on physical examination and DFC and TMT1- angle and

DFC respectively.

The mean DFC for all feet was 18 mm (SD±5.6), with a range of 7.4 - 28 mm. Classifying the

various foot types according to physical examination, mean DFC for the group with flatfeet

was 15 mm (SD 4.5). The mean DFC for the group with normal feet was 20 mm (SD 4.8) and

for the group with cavus feet the mean DFC was 22 mm (SD 5.4) (Figure 8).

Table 2. Descriptive and reliability numbers for the footprint measurements and radiographic angles (for all correlations p< 0.05)

TMT-angle (n=23) CI-angle (n=28)

Mean (SD) 0.1 (±9.8) 21 (±6.1)

Min -17 12

Max 20 33

Classification 9 flat arch6 normal arch8 high arch

13 flat arch12 normal arch3 high arch

Intra-observer reliability observer 1

0.98 (95%CI: 9.94-0.99) 0.99 (95%CI: 0.97-0.99)

Intra-observer reliability observer 2

0.98 (95%CI: 0.96-0.99) 0.99 (95%CI: 0.98-1)

Inter-observer reliability

0.91 (95%CI: 0.74-0.97) 0.98 (95%CI: 0.96-0.99)

Correlation with physical examination

0.77 0.72

Table 3. Pearson’s correlations between DFC and different variables. (*statistically significant with p <0.05)

Correlations (n=28) DFC (Distance Fibula-Calcaneus)

Physical examination 0.54*

TMT-angle 0.60*

CI-angle 0.59*

Shoe size of volunteers 0.39*

Length of volunteers 0.09

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The ANOVA-test showed a significant difference of the DFC within the three different foot

type groups (p<0.05). Additionally, the Bonferroni multiple comparisons test revealed a

significant difference for the DFC between the group with flat feet and the group with cavus

feet (p=0.01). However, the same test did not reveal a significant difference for the DFC

between the group with flat feet and normal feet (p=0.07). Also, no significant difference

for the DFC was found between the group with normal feet and the group with cavus feet

(p=1.0).

DiscUssioN

The DOPP demonstrated to be a reliable instrument and radiological measurements for DFC

were highly reliable. The most important findings were that portal location in patients with

a flat foot should be placed at a mean of 15 mm from the tip of the fibula, in normal feet at

20 mm, and in cavus feet at a mean of 22 mm distal to the tip of the fibula.

Because ultimately most orthopaedists will determine foot type through physical examina-

tion, the most important correlation of the DFC is with foot morphology according to the

physical examination and not the TMT-1 angle. The loss of 5 patients for measuring the TMT

angle is a limitation of our study.

Our presumption that as the calcaneus inclines, the DFC gets larger seems evident. However,

correlation between the DFC and the CI-angle was moderate. Furthermore, not all volunteers

Figure 8. Mean distance for foot type according to physical examination. The distance shows marked overlap all three foot morphologies; there was no significant difference between the distance in flat- and normal or normal- and cavus feet. The Bonferroni multiple comparisons test did reveal a significant dif-ference for the DFC between the group with flat feet and the group with cavus feet (p=0.01)

186

with cavus feet showed a high CI- angle. This may be due to the fact that cavus is not always

associated with a large CI-angle13. As a result of that, the distance of the posterosuperior

calcaneus to the tip of the fibula is smaller than we expected in several cases. Also reported

is that some volunteers with a normal foot shape showed a rather high CI-angle. Due to

hyperpronation, some feet appeared to be flat feet, where hyperpronation and flat feet are

two different morphologies that can co-exist. In these cases, on physical examination foot

shape was normal with a radiographic high CI-angle, rendering a larger than expected DFC.

This could explain why there is marked overlap of DFCs between the group with normal feet

and the group with cavus feet.

Correlation between physical examination and DFC was also moderate so that a numeric

scale for portal placement based on foot morphology (angles) could not be constructed

from our study. Apparently, the various foot types show a marked overlap between the

distances from calcaneus to fibula. We can conclude however that in flat feet portal location

is significantly more proximal to the tip of the fibula, when compared to cavus feet. We real-

ize that we included a limited amount of volunteers; with a larger population we might also

find a significant difference between the DFC in flat and normal- and normal- and cavus feet.

The DOPP demonstrated to be highly reliable; with the limitation that only one observer

handled the DOPP throughout the whole study. Future research is still needed to determine

the inter-observer reliability for using the DOPP, and thereby its validity. The next step could

be testing the correlation of the DFC as measured pre-operatively with measurements of the

distance of the fibula tip to the incision as placed by an experienced orthopaedist. When

correlation is high, the DOPP might eventually be implemented in the daily clinic on individual

patients with a retrocalcaneal bursitis scheduled for EC. Until then, when uncertain about

portal placement, using fluoroscopy can be considered.

coNcLUsioN

The DOPP demonstrated to be highly reliable in measuring the DFC (ICC= 0.99). A numeric

distance scale for use in all different foot morphologies could not be constructed. There is a

direct relation between portal location and foot morphology (p<0.05), as in flat feet portal

location is significantly more proximal (15 mm) to the tip of the fibula when compared to

cavus feet (22 mm).

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12. Murley GS, Menz HB, Landorf KB. A proto-

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PArt v GeNerAL DiscUssioN

General discussion

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termiNoLoGY

The best possible management of different pathologies begins with universal language in

science and daily clinical practice. Uniform terminology is believed to provide us with higher

consistency and understandability of a problem and therefore ensures that information can

be shared and compared seamlessly amongst clinicians. In chapter 1 a new terminology

for Achilles tendon related disorders was proposed, including the combination of anatomic

location, symptoms, clinical findings and pathological changes for each entity. Examining

the evolution of terminology over the last century, the ways to describe a clinical problem

became endless and eponyms received pole position. The reasoning behind a change in

terminology is unclear; it may for example be caused by different interpretation of pathology.

However, constructing terminology in which Haglund’s deformity, - syndrome and -disease

are all dissimilar entities is not desirable. The use of improper terms however is acquired over

centuries and may be complex to cure. Restrain is advocated regarding the adoption of new

terms or modify a pre-existent terminology solely on personal preference or interpretation.

oUtcome meAsUres AND AssessmeNt tooLs

In 2001 Tallon et al published a review on the outcome after surgery in patients with chronic

Achilles tendinopathy74. They pointed at the deficiencies in outcome assessment and criteria,

and subsequently recommended the use of outcome measures that were condition-specific,

reliable, sensitive, and correlated with clinical severity. Outcome assessment tools provide

the opportunity for universal outcome reporting. Data collected at widespread points can

then be fairly compared, and common goals of therapy can be determined. In chapter 2 a

summary is given of the available outcome measures and assessment tools. Assessment tools

described are strength measurements with dynamometry, endurance- and jump testing.

Strength measurements have shown to be reliable and valid for measuring improvement in

strength, but are curiously not useful in a clinical setting as they do not correlate sufficiently

with (subjective) functional performance13. The normal number of heel rise repetitions in

muscular endurance testing ranges from 25-7048. Therefore only a difference over time can

be measured and again there is no correlation with initial functional performance. This also

accounts for jump tests used to evaluate loading of the Achilles tendon. Assessment tools do

not correlate with initial functional performance, but are useful in measuring the effective-

ness of a treatment modality. The subjective VISA-A score is recommended for scientific

purposes as it has good reliability and validity, and has now been used in at least 19 different

studies16,18,20.

In chapter 3, after the German, Swedish and Italian, the VISA-A questionnaire was trans-

lated to the Dutch language (VISA-A-NL) and tested for reliability, internal consistency, con-

struct- and content validity. Application to non- athletes was also evaluated. The VISA-A-NL

194

showed high reliability (0.97 (95% CI 0.95-0.98)). Reliability of the translation was excellent,

with a statistically not significant difference between assessments. Crohnbach’s alpha for

internal consistency was good at 0.80. It even increased to 0.88 without the activity domain

of the questionnaire, accounting for 40% of points. As approximately 30% of patients do

not participate in sporting activities10 we concluded that patients with a non-athletic history

should receive a modified VISA-A score from which questions 7 and 8 are deleted, especially

as the effect of treatment in non-athletes otherwise can be underestimated.

Correlation of the VISA-A-NL with other subjective questionnaires (VAS, FAOS, SF-36) and

the AOFAS only was good compared with the functional subscale of the SF-36. Correlation

with other questionnaires was moderate or poorer. Noticeable is the moderate correlation

with VAS, with is a validated subjective outcome measure frequently used for scientific

means63. Although the FAOS has shown to be responsive to changes over time65, it has not

been validated for Achilles tendinopathy. To constructively discuss this matter these question-

naires first need to be validated for Achilles tendinopathy. We decided not to, as filling out

larger amounts of paperwork would be a burden for patients, with a lower response rate as

a consequence.

miDPortioN AchiLLes teNDiNoPAthY: cAUse of PAiN AND treAtmeNt moDALities

Numerous treatment modalities for midportion Achilles tendinopathy have been reported

over the last decades. However, only few (e.g. eccentric training) render a good outcome.

Unsatisfactory treatment results can be caused by the reality that the mechanisms by which

these diverse treatments attack pathology are unclear. Moreover, the mechanism by which

the problem originates is even unidentified. In other words: should we not first identify the

problem before coming up with a solution?

When work on this thesis started, one of the newest treatment modalities for midportion

Achilles tendinopathy was Ethoxysclerol as introduced by Alfredson et al.5-8,36,79. Etoxysclerol

damages the intima of bloodvessels after which they obliterate. The theory on which the

injection of this substance was built, neovascularisation and accompanying neo-innervation

in and around the tendon as the cause of complaints, also broke new ground and formed

the basis of current new insights. The godfathers of Etoxysclerol treatment instructed our

team and from 2004-2007 a total of 113 consecutive patients with 140 symptomatic Achilles

tendons underwent colour Doppler ultrasonography investigation (US) in our clinic. Sixty-two

patients had 70 symptomatic tendons showing neovascularisation (50%). In 50% of tendons

with Achilles tendinopathy no neovessels were found. Others found neovascularisation in

50-88% of symptomatic tendons23,62,64,78.

If only present in 50% of tendons, can neovessels yet be the cause of complaints? Or do

they obliterate in the progress of pathology or healing?

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Furthermore, of these patients only 44% of tendons were painless or minimally painful

at six weeks after treatment. At 2.7-5.1 year follow-up 53% of all treated tendons had

undergone various forms of additional treatment (conservative or surgical). Three patients

still had complaints. Can we conclude from this study, combined with Paavola et al.59 that

whatever treatment is commenced, that on the long term the natural history is benign?

The main focus of treatment of Achilles tendinopathy is on relieving pain. It is question-

able if degeneration of the tendon itself is the main cause of pain, since intratendinous

changes are found in up to 34% of people without complaints27,33,40, 42. Persistent structural

abnormalities and thickening of the tendon 13 years after intra-tendinous surgery for Achil-

les tendinopathy was seen, whereas all patients were satisfied with the results and went back

to Achilles tendon loading activities without restrictions9. Degeneration had not completely

resolved, and although ruptured tendons show degenerative changes on histology41, there

is no evidence that pathological tendons are more prone to rupture. On the contrary, most

often intratendinous changes are addressed in surgical treatment. But are these changes

responsible for the pain?

Chapter 8 comprises a philosophy of the cause of pain in midportion Achilles tendinopa-

thy. It is postulated that the process of tendinopathy does start with localized tendon micro-

injury and degeneration, caused by ageing and repetitive strain. The pain is often prominent

at 2-7 cm proximal to the calcaneus, where the tendon makes a twist; it is described that

at this site blood flow even declines10,58. When the demands of the tendon exceed fiber

strength, micro-injuries can develop1. An inadequate repair process causes a repetitive cycle

of inadequate collagen and matrix production, tenocyte disruption, a further decrease of

collagen and matrix and consequently increased vulnerability to further micro-injuries. Due

to the lack of vascularisation, instead of a chemical-, a neurogenic inflammatory process is

activated to repair these microruptures.

This neurogenic inflammatory response comprised of a new ingrowth of nerve fibers15,28

accompanying the peritendinous vascular ingrowth from the paratenon into the tendon

proper46,67. With this nerve ingrowth, levels of glutamate, calcitonin gene-related peptide

(CGRP) and substance P rise2,11. Sensory neonerves cause an increase in pain signalling by

producing these nociceptive substances past the critical threshold4,11. Transition to symp-

tomatic tendinopathy now occurs. Also, myofibroblasts proliferate and synthesize abundant

amounts of collagen to repair the tendon proper, but also cause the formation of scar tissue

around the tendon and consequently the paratenon adheres onto the Achilles tendon at

the location of the neurovascular ingrowth. Scarring in turn may lead to impaired circulation

and further contribute to the pathogenesis of Achilles tendinopathy. In the earlier described

20-50% of patients without neovascularisation, vasoconstriction and scarring with mechani-

cal constriction may already have lead to obliteration of neovessels. Nerves however will

survive.

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Involvement of the plantaris tendon in the process of tendinopathy is considered, as it runs

with the Achilles tendon on its medial side within a shared paratenon. When constriction

of the paratenon develops, the plantaris tendon gets involved. As described, it is tri-articular

and the medial side of the midportion of the Achilles tendon is bi-articular, hypothetically

causing altered mechanics and pain as a consequence. Recently Lintz et al. performed a

biomechanical study indicating that the Achilles tendon elongates a greater distance than

the plantaris tendon under similar tensile stresses. As a consequence the two surfaces could

trap peritendinous tissues between them, which could be subject to shear stresses and cause

pain47.

In chapter 5 Achilles tendoscopy as invented by van Dijk et al. in 1997 is described75. The

paratenon is endoscopically released from the Achilles- and plantaris tendon is cut with good

clinical results. Alfredson et al. recently described a series of 73 Achilles tendons in which

during treatment with ultrasound and Doppler-guided scraping an invaginated, or close by

located, enlarged plantaris tendon was found in 58 of cases3. In these patients, the plantaris

tendon was surgically removed with good clinical results and the authors confirm that the

plantaris tendon might be of interest in the aetiology and treatment of midportion Achilles

tendinopathy.

However, large comparative studies are lacking as the population in the academical

setting is small, and patients demanding surgery even less. Ideal would be a randomized

clinical trial comparing open surgery with endoscopic release of the paratenon and a group

undergoing the endoscopic approach as well as transsecting the plantaris tendon. Currently

a prospective study on Achilles tendoscopy is being carried out. However, involvement of

the plantaris tendon in the pathological process had not yet been studied anatomically nor

clinically in an isolated procedure.

In chapter 6 it is hypothesized that constriction of the paratenon onto the Achilles

tendon consequently causes adhesion of the plantaris tendon to the surrounding tissues.

After formation of adhesions, the different mechanical properties of both the Achilles- and

plantaris musculotendinous complex may be the cause of complaints. However, absence

of the plantaris tendon in 7-20% of human cadavers has been described21,22,30,32,54,68. An

observational study of 107 lower extremities on the anatomy at the level of the Achilles

tendon was conducted. In all a plantaris tendon was identified, which was occasionally

difficult due to a mixture of 9 different insertion sites, especially the variant with insertion

into the medial side of the Achilles tendon proper. However, when dissecting from proximal

to distal it was identified in all specimens. This could be an explanation for the tentative

absence in the earlier mentioned 7-20% of legs. Another explanation could be absence due

to isolated rupture25,35. With our relatively large group of specimens, we not only contradict

earlier findings of its absence, but also raise implications for daily practise. The plantaris

tendon is often used for grafting because it can be sacrificed without discernible deficit, and

is of adequate length and thickness for many applications14,49,53,69. We advise to retrieve the

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tendon proximally (e.g. with a tendon stripper). The use of ultrasound- or MR- imaging prior

to surgery to pre-assess its course may be helpful.

In 11 specimens (10%) firm connections were found at the level of the Achilles tendon

midportion. It was not possible to perform histology of these findings, or of the involved

Achilles tendons, a flaw of this study.

Chapter 7 illustrates a pilot study of a new surgical technique in which the plantaris

tendon is excised with a hamstring stripper through a small incision on the medial side of the

proximal calf. Three patients with complaints of midportion tendinopathy were treated in this

pilot. Although the tendon stripper appeared too short in one patient, the plantaris tendon

ruptured above the adhesions in the other, and in one the procedure went as planned, all

were satisfied with the result and reported no complaints at 1 year follow-up. This outcome

may well be attributable to coincidence as only 3 patients were treated. Although the pro-

cedure went with varying success, different pull of adhered tendons was eliminated in all by

excising the tendon. Another explanation for pain relief could be indirect stripping of the

paratenon with introduction of the tendon stripper.

Now where should the treatment of Achilles tendinopathy commence? Should the plan-

taris tendon be (surgically) addressed, or should the sympathetic nerves coming from the

paratenon be denervated? What is effective in pain relief in the majority of patients?

Of course direct referral to surgical measures is undesirable. Conservative management

should always be considered first. Injection with Etoxysclerol, saline and PRP could theoreti-

cally yield similar results as surgical denervation. With Etoxysclerol, nerves are probably also

attacked. On the contrary, injection may not suffice because of low volume and effectiveness

of the substance on nerves, and adhesions may be too solid to be adequately released. High-

volume injection has been successfully performed, thereby obliterating neovascularisation

and accompanying neonerves18. Brisement, first described in 199739, was initially meant to

interrupt the degenerative cycle of the tendon proper by initiating a healing cascade, but in

essence seems equivalent to current high-volume injections.

Moreover, small volume injections also seem to generate a response. Injection of PRP

was compared with saline, producing an equivalent outcome24. Corticosteroid injections for

lateral epicondylitis and aprotinin for Achilles tendinopathy were comparable with placebo,

showing no statistically significant difference in outcome70. Could this mean that no matter

what we introduce, an inflammatory response will be generated?

Surgical treatment should be reserved for patients that do not respond to primary con-

servative measures. When sufficiently researched in well-designed clinical trials early surgical

management can be considered for professional athletes or patients depending on their

fitness in daily life for a quicker return to normal activities.

198

retrocALcANeAL BUrsitis: DiAGNosis AND treAtmeNt

A symptomatic inflammation of the retrocalcaneal bursa is caused by repetitive impingement

of the bursa between the anterior aspect of the Achilles tendon and a bony posterosuperior

calcaneal prominence26,71,72. Most publications focus on this prominence, which however

has not shown to be very reliable17,29,61. In retrocalcaneal bursitis, the normally sharply

outlined radiolucent retrocalcaneal recess of Kager’s triangle is obliterated. In chapter 9

we determined the usefulness and reliability of the radiographic appearance of this recess

in diagnosing a retrocalcaneal bursitis on digital radiographs. The sensitivity was 83% for

observer 1 and 79% for observer 2. Specificity was 100% and 98% for observer 1 and 2. The

interobserver reliability test calculated a kappa-value of 0.86. For observer 1 intraobserver

reliability was 0.96 and 0.92 for observer 2. This means further diagnostic evaluation is not

necessary, resulting in a higher cost-effectiveness and quicker treatment. MRI can still be per-

formed in case of doubt. However, does Kager triangle normalize when complaints diminish?

If yes, is the retrocalcaneal recess useful for diagnosis when complaints unhoped-for recur?

Kager’s triangle is distorted due to the inflammatory response after surgical treatment; in

endoscopic surgery the flow of saline also causes distortion. Scar tissue develops which also

causes a change in radiolucency, one that over time might diminish. Research on the useful-

ness of Kager’s triangle after surgery is currently executed.

An optimal treatment algorithm for retrocalcaneal bursitis, as for midportion tendinopathy,

has not been found yet. Conservative management includes inlays, adaptation of shoe wear,

rest, NSAIDs and a single cortisone injection in the retrocalcaneal bursa56,57,73. Cortisone

injections are not advised since these can weaken the tendon with the potential danger of

rupture. The best level of evidence for this potential danger nevertheless is derived from case

reports19,34,43,50,77.

The aim of surgery for retrocalcaneal bursitis is to prevent impingement of the bursa

between the Achilles tendon and the calcaneus. This can be accomplished by removing the

inflamed retrocalcaneal bursa, followed by either resection of the posterosuperior tuberosity

or by a closing wedge osteotomy to prevent recurrence. Posterosuperior calcaneal resection

can be performed through a posterolateral or posteromedial incision or through a combina-

tion of both12,44,60.

Due to inappropriate visualization of the Achilles tendon during open procedures, weaken-

ing or even rupture has been reported45,52. Full recovery time after open resection can take

up to 2 years.

Endoscopic calcaneoplasty offers a minimally invasive alternative to open surgery. Sur-

geons familiar with the endoscopic approach favor this procedure, because of its better

visualization. Our results of endoscopic calcaneoplasty are comparable with other reports

on endoscopic treatment31,37,38,66,76. Two portals are used, just lateral and medial to the

Achilles tendon, at the level of the posterosuperior tuberosity of the calcaneus. During the

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procedure, the inflamed retrocalcaneal bursal tissue and posterosuperior prominence of the

calcaneus are resected using a Bonecutter shaver. However, due to the local anatomy, bulky

subcutaneous tissue and swelling of the bursal tissue, palpation of the posterosuperior tuber-

osity is difficult and portals can easily be placed too proximal. This will result in a suboptimal

procedure. Fluoroscopy is sometimes used to make portals, but can be time-consuming as

the surgeon has to rely on availability and personnel. We therefore aimed to standardize

portal placement using a self-developed ‘Device for Optimal Portal Placement’ (DOPP), using

the distance from the distal tip of the fibula to the posterosuperior calcaneus (DFC) on a

radiograph in volunteers as described in chapter 11. This tip has not been validated but is

already used as a landmark for portal placement in standard 2-portal hindfoot endoscopy

with good visualization. It was decided to use healthy volunteers, as the goals of this study

were to 1) validate the DOPP for portal placement, 2) see if the distance DFC would help us

determine the ultimate position of portals and 3) to recover a direct relationship between

foot morphology and portal location. If standardization was performed in retrocalcaneal

cases, many patients would have been needed as there is a large between- patient variance

in calcaneal contour in retrocalcaneal bursitis.

However, from this study a numeric distance- scale to be used in all different foot mor-

phologies could not be constructed. Although TMT1, -CI-angles and physical examination

were found to be the best available objective measures to determine foot morphology51,55,

disappointing correlations were found. Apparently, the various foot morphologies show a

marked overlap between the distances from posterosuperior calcaneus to fibula. We can

conclude however that in flat feet portal location is significantly more proximal to the tip of

the fibula, when compared to cavus feet. Still a limited amount of volunteers was included;

with a larger population we might also find a significant difference between the DFC in flat

and normal- and normal- and cavus feet and construction of a numeric scale may be possible.

The DOPP demonstrated to be highly reliable; with the limitation that inter-observer reli-

ability was not tested. Future research is still needed to determine its validity. The project

could be extended with a larger amount of volunteers. The next step could be testing the

correlation of the DFC as measured pre-operatively with measurements of the distance of

the fibula tip to the incision as placed by an experienced orthopaedist. When correlation is

high, the DOPP might eventually be implemented in the daily clinic on individual patients

with a retrocalcaneal bursitis scheduled for EC; or a gliding scale for portal placement may

be constructed. Until then, when uncertain about portal placement, fluoroscopy should still

be considered.

fUtUre reseArch

Research on Achilles tendon-related problems is ongoing. The first step to optimal manage-

ment is to speak the same scientific language. This not only accounts for the Achilles tendon,

200

and therefore it is advocated to construct a standard terminology for all medical problems.

Implementation however will be complex. Further research on chronic midportion Achilles

tendinopathy should focus on the cause of pain instead of formulating more substances for

injection in or around the tendon as currently seems to be the tendency. Recognizing the

cause of complaints will help to further define therapeutic strategies. Undoubtedly, caution

should be taken when considering surgical treatment, although endoscopic and minimally

invasive procedures generate considerably less complications and shorter rehabilitation when

compared to open surgery. Treatment in my opinion therefore needs to be individualized.

Currently patients spend months to even years in the medical circuit. This also accounts for

patients with retrocalcaneal bursitis. Surgery is less often considered in non-athletes with low

demands in daily life and minor complaints, but endlessly applying conservative measures in

athletes and patients with high daily physical demands requiring a quick return to normal

activities may be unwanted. In minimally invasive and endoscopic surgery for midportion

tendinopathy the degenerative lesion is often left untouched, of which it would be interest-

ing to research the long-term consequences.

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PArt vi

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GeNerAL iNtroDUctioN

The prevalence of obesity in the Western World is rising, and therefore getting- and keep-

ing fit has been increasingly important in the recent years. Endurance sports like triathlons

and long distance running have gained popularity. Overuse injuries have become prominent

in daily practice. General inactivity during the week followed by extreme exercise in the

weekend allow for these types of injury to occur. 30-50% of all sports injuries are overuse

injuries. Chronic Achilles tendon pathology is one of the biggest problems in sports involving

running and jumping. In elite long-distance runners there is a lifetime risk of 52% of sustain-

ing an Achilles tendon injury. However, it is not always related to excessive physical activity.

Thirty percent of patients have a sedentary lifestyle. Recalcitrant Achilles tendons may cause

pain for years and are often resistant to any form of treatment. In the end, chronic Achilles

tendon complaints may be self-limiting. Especially athletes will not consent with this possible

prospect. The cause of pain has not yet been clarified, and therefore its treatment is chal-

lenging and often unsatisfactory. The aim of this thesis was to elucidate the cause of pain,

to develop appropriate assessment tools, to invent minimally invasive treatment methods,

and to optimize diagnostic and endoscopic methods for chronic Achilles tendon problems.

chAPter 1

Terminology for Achilles tendon related disordersThe terminology of Achilles tendon pathology has become inconsistent and confusing

throughout the years. A new terminology is proposed; definitions include the anatomic loca-

tion, symptoms, clinical findings and histopathology.

Midportion Achilles tendinopathy: a clinical syndrome characterized by a combination

of pain, swelling and impaired performance. It includes, but is not limited to, the histo-

pathological diagnosis of tendinosis. Achilles paratendinopathy: an acute or chronic inflam-

mation and/or degeneration of the thin membrane around the Achilles tendon. There are

clear distinctions between acute paratendinopathy and chronic paratendinopathy, both in

symptoms as in histopathology. Insertional Achilles tendinopathy: located at the insertion of

the Achilles tendon onto the calcaneus, bone spurs and calcifications in the tendon proper at

the insertion site may exist. Retrocalcaneal bursitis: an inflammation of the bursa in the recess

between the anterior inferior side of the Achilles tendon and the posterosuperior aspect of

the calcaneus (retrocalcaneal recess). Superficial calcaneal bursitis: inflammation of the bursa

located between a calcaneal prominence or the Achilles tendon and the skin.

Finally, it is suggested that previous terms as Haglund’s disease; Haglund’s syndrome;

Haglund’s deformity; pump bump (calcaneus altus; high prow heels; knobbly heels; cucum-

ber heel), are no longer used.

212

chAPter 2

Outcome measures and assessment toolsThorough history taking and clinical examination are essential in diagnosing Achilles tendi-

nopathy. Moreover, it is important to continuously evaluate the patients’ progress with both

validated subjective scoring systems, such as the VISA-A questionnaire, and with various

validated functional tests. Also, general subjective complaints and ability to return to previ-

ous physical activity and sports are important outcome measures. Proper evaluations with

validated tests are not only of importance for scientific purposes, but also to the practitioner

and the patient to follow the progress with treatment and rehabilitation.

chAPter 3

Translation and validation of the Dutch VISA-A questionnaire for Achilles tendinopathy and applicability to non-athletesIn 2001, the Victorian Institute of Sports Assessment developed a self-administered question-

naire evaluating symptoms and their effect on physical activity for patients with Achilles

tendinopathy. It has proven to be an effective outcome questionnaire in various languages.

The aim of this project is to translate and validate the VISA-A questionnaire into the Dutch

language (VISA-A-NL) and to assess its applicability to non-athletes. After translation accord-

ing to a forward-backward protocol, 101 patients with complaints of Achilles tendinopathy

were asked to fill out the VISA-A-NL at two time points together with VAS, FAOS and SF-36

questionnaires. Reliability, internal consistency, construct- and content validity were tested.

The VISA-A-NL proved to be an excellent evaluation instrument for the Dutch physician. If

applied to non-athletes, using a modified score (questions 1-6) is recommended. Correlation

of VISA-A-NL with other questionnaires was moderate or poorer.

chAPter 4

Less promising results with sclerosing Ethoxysclerol injections for Achilles tendinopathy: a retrospective studyIn patients with complaints of chronic midportion Achilles tendinopathy, neovascularisation

around the Achilles tendon and structural changes in the area were observed, but not in pain

free normal tendons. Local injections of the sclerosing substance Polidocanol (Etoxysclerol)

have shown to yield good clinical results in patients with chronic Achilles tendinopathy. After

training by the inventors of the technique, sclerosing Etoxysclerol injections were applied to

48 patients (53 tendons) in our center. Six weeks after the last injection, only 44% has less

or no complaints. At 2.7-5.1 year follow-up, 53% had received additional treatments, and

3 of these patients (7.5%) still had complaints of Achilles tendinopathy. We were therefore

Part VI

Sum

mary

213

not able confirm the high beneficial value of sclerosing neovascularisation in patients with

Achilles tendinopathy.

chAPter 5

Tendoskopie am Sprunggelenk und FußIn contrast to arthroscopy, which has become the preferred technique to treat intra-articular

ankle pathology, extra-articular problems of the ankle have traditionally demanded open sur-

gery. Open ankle surgery has been associated with complications such as injury to the sural

nerve or superficial peroneal nerve, infection, scarring, and stiffness of the ankle joint. The

percentage of complications reported with open surgery for e.g. posterior ankle impinge-

ment varies between 15 and 24%. The incidence of these complications has stimulated

the development of extra- articular endoscopic techniques. Endoscopic surgery offers the

advantages related to any minimally invasive procedure, such as fewer wound infections,

less blood loss, smaller wounds and less morbidity. Aftertreatment is functional, and surgery

is performed on an outpatient basis.

Tendoscopy can be performed for the treatment and diagnosis of various pathologic con-

ditions, as described in this chapter. In Achilles tendoscopy the paratenon and the plantaris

tendon are released, leaving the tendon proper untouched. This procedure results in a good

outcome on short- and midterm follow-up.

chAPter 6

Relationship between the plantaris tendon and the Achilles tendon: an anatomical study Pain in midportion Achilles tendinopathy is often most prominent on the medial side, where

degenerative changes are also most often found. During Achilles tendoscopy, we find that

the plantaris tendon is fixed to the Achilles tendon at the level of complaints. In chronic

inflammation, adhesions between Achilles- and plantaris tendon, running collectively in the

paratenon, may be formed. The Achilles tendon is involved in plantarflexion, whereas the

plantaris tendon also contributes to ankle inversion. These opposite forces may cause pain

in case of adhesions. The purpose of this study was to assess the anatomical position of the

plantaris tendon and its relationship with the Achilles tendon. In all specimens a plantaris

tendon was identified. 9 different sites of insertion were found, mostly medial and fan-

shaped onto the calcaneus. In 11 specimens attachments between Achilles- and plantaris

tendon were found at the level of complaints which may contribute to pain.

214

chAPter 7

Good outcome after stripping the plantaris tendon in patients with chronic midportion Achilles tendinopathyAchilles tendinopathy is a problem that is generally difficult to treat. The pain is frequently

most prominent on the medial side of the midportion of the tendon, where the plantaris

tendon is running parallel to the Achilles tendon. The purpose of this study was to assess if

excision of the plantaris tendon would relieve symptoms. Three patients with pain and stiff-

ness at the midportion level of the Achilles tendon were treated by excision of the plantaris

tendon. Pre-operatively these patients experienced recognisable tenderness on palpation of

the medial side of the midportion of the Achilles tendon with localized nodular thickening

at 4-7 cm proximal to the insertion. MRI indicated Achilles tendinopathy with involvement of

the plantaris tendon. The plantaris tendon was bluntly retrieved and excised with a tendon

stripper through a 3 cm incision in the proximal calf. We report a good outcome of this

novel procedure in 3 patients with chronic midportion Achilles tendinopathy. The medial pain

might be based on involvement of the plantaris tendon in the process, but well-designed

studies need to be performed to confirm our hypothesis.

chAPter 8

Midportion Achilles tendinopathy: why painful? An evidence based philosophySeveral factors play a role in the cause of pain in a patient with midportion Achilles tendi-

nopathy. When the demands of the tendon are higher than can be managed, micro-injuries

develop. The body reacts with a repair process, which is inadequate in patients developing

tendinopathy. This inadequate repair causes a repetitive cycle of inadequate collagen and

matrix production, tenocyte disruption, a further decrease of collagen and matrix and an

increased vulnerability to further micro-injuries. Vascular ingrowth to repair the defect arises

from the paratenon. These bloodvessels are accompanied by sensory neonerves, causing an

increase in pain signaling by producing nociceptive substances past the critical threshold.

Myofibroblasts proliferate which synthesize abundant amounts of collagen to repair the ten-

don proper, but also cause the formation of scar tissue around the tendon and consequently

adhesions of the paratenon onto the Achilles tendon at the location of the neurovascular

ingrowth. Scarring in turn may lead to obliteration of neovessels, impaired circulation and

further contribute to the pathogenesis of Achilles tendinopathy, meaning that there is no

further action towards repair. Nerves however will survive. Pain is often most prominent on

the medial side of the midportion Achilles tendon. At this level, the plantaris tendon runs

closely with- and parallel to the Achilles tendon. Adhesions between both tendons obstruct

the opposite forces of these two bi- and tri-articular muscle groups. Repetitive traction onto

Part VI

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this richly innervated area might contribute to the medially located pain and stiffness during

and after walking.

chAPter 9

Appearance of the weight-bearing lateral radiograph in retrocalcaneal bursitisA chronic retrocalcaneal bursitis is caused by repetitive impingement of the retrocalcaneal

bursa between the Achilles tendon and posterosuperior calcaneus. On physical examination,

a prominent swelling is palpable lateral and medial from the Achilles tendon just proximal to

the calcaneus. Standard lateral and anteroposterior radiography of the ankle is performed

to assess foot deformities or bony abnormalities. To confirm diagnosis, ultrasound, MRI or

even bone scans are performed. This chapter shows that a visible soft tissue swelling in the

retrocalcaneal recess on standard lateral weight-bearing radiographs of the ankle is useful

in diagnosing a retrocalcaneal bursitis and that expensive and time- consuming additional

imaging is no longer necessary.

chAPter 10

Endoscopic calcaneoplastyWhen a retrocalcaneal bursitis is confirmed and maximum conservative treatment fails,

surgery is considered. Most often open procedures are performed; however, in our clinic the

endoscopic calcaneoplasty was invented. Two portals are used, just lateral and medial to the

Achilles tendon, directly proximal to the superior part of the calcaneus. During the proce-

dure, the retrocalcaneal bursa, posterosuperior tuberosity of the calcaneus and synovitis are

resected. Aftertreatment is functional and patients can resume their normal activities.

chAPter 11

Optimization of portal placement for endoscopic calcaneoplastyDue to the local anatomy and swelling palpation of the superior part of the calcaneus can be

difficult and portals can be placed too far proximal. The calcaneus in these cases cannot be

reached properly resulting in a suboptimal procedure or, when the problem is recognized, a

need to replace or lengthen the incisions. In this chapter, we measured the distance from the

tip of the fibula to the posterosuperior calcaneus in different foot morphologies, as a tool for

accurate portal placement. Portal location in patients with a flat foot should be at a mean of

15 mm from the tip of the fibula, in normal feet at 20 mm, and in cavus feet at a mean of 22

mm distal to the tip of the fibula. The various foot types show a marked overlap between the

216

distances from calcaneus to fibula, however we can conclude that in flat feet portal location

is significantly more proximal to the tip of the fibula, when compared to cavus feet.

GeNerAL DiscUssioN

Before treatment of different types of Achilles tendinopathy can be optimized, some basic

issues need to be taken into account. First, we all need to start speaking the same language,

which is important in both science and daily clinical practice. Worldwide standard terminol-

ogy and validated outcome measures for both athletes- and non-athletes are important first

steps. Secondly, the cause of complaints needs to be found. As is evidently the major concern

in any pathology, it would help us define more accurate and individualized treatment strate-

gies. Sclerosing neovessels did not seem to be the solution. It was tried to get focus off

the intratendinous changes in midportion tendinopathy by formulating an evidence- based

philosophy on the involvement of the paratenon and plantaris tendon. More research is

needed to confirm this hypothesis.

In retrocalcaneal bursitis MRI is no longer indicated if the patient is appropriately assessed

clinically and digital radiographs are available. The value of radiography after previous hind-

foot surgery is currently under investigation. Portal placement in endoscopic calcaneoplasty

needs to be standardized as swelling and local anatomy prevent proper assessment. In

patients with flat feet portals should be placed more proximal than in cavus feet; further

research with a higher number of patients is needed to find significant differences between

all foot morphologies. Until then, for surgeons less familiar with the procedure fluoroscopy

is advocated.

Samenvatting

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ALGemeNe iNtroDUctie

Omdat de prevalentie van obesitas in de Westerse wereld stijgt, is fit worden en –blijven

de afgelopen jaren toenemend belangrijk geworden. Duursport als triatlons en hardlopen,

worden steeds populairder en overbelastingsblessures komen vaker voor in de dagelijkse

praktijk. Dit type blessures wordt veroorzaakt door relatieve inactiviteit op doordeweekse

dagen op kantoor, gevolgd door extreme trainingen in het weekend. 30-50% van alle sport-

letsels zijn overbelastingsblessures. Chronische Achillespees pathologie is één van de meest

voorkomende gevolgen van hardlopen en springsporten. In elite langeafstandslopers is er

tijdens een leven een risico van 52% om een Achillespeesblessure op te lopen. Dit probleem

is niet altijd gerelateerd aan sporten, zelfs 30% van de populatie bestaat uit patiënten die

een voornamelijk zittend leven leiden. Weerspannige Achillespezen kunnen jarenlang pijn

veroorzaken en zijn meestal resistent tegen elke vorm van behandeling. Uiteindelijk gaan

de klachten mogelijk vanzelf weer over, maar zeker atleten zullen niet instemmen met een

afwachtend beleid. Omdat de oorzaak van de pijn tot dusver nog niet opgehelderd is, is de

behandeling een onbevredigende uitdaging. Het doel van dit proefschrift was het ophelderen

van de oorzaak van de pijn, het ontwikkelen van geschikte beoordelingsinstrumenten, het

uitvinden van minimaal invasieve behandelmethoden, en het optimaliseren van diagnostische

en endoscopische werkwijzen voor chronische Achillespeesproblemen.

hoofDstUk 1

Terminologie voor problemen gerelateerd aan de AchillespeesTerminologie voor het omschrijven van Achillespees pathologie is door de jaren heen verand-

erlijk en verwarrend gebleken. Een nieuwe terminologie wordt in dit hoofdstuk voorgesteld:

definities omvatten anatomische locatie, symptomen, klinische bevindingen en histopatholo-

gie.

Midgedeelte Achilles tendinopathie: een klinisch syndroom gekarakteriseerd door een

combinatie van pijn, zwelling en verminderde prestatie. Het omvat, maar is niet beperkt

tot de histopathologische diagnose van tendinose. Achilles paratendinopathie: een acute of

chronische inflammatie en/ of degeneratie van het dunne membraan rond de Achillespees.

Er zijn duidelijke verschillen tussen acute paratendinopathie en chronische paratendinopathie

in symptomatologie en histopathologie. Insertie tendinopathie: gelocaliseerd bij de insertie

van de Achillespees aan de calcaneus, tractiesporen en calcificaties in het peeslichaam ter

plaatste van de insertie kunnen aanwezig zijn. Retrocalcaneaire bursitis: een inflammatoir

proces van de bursa in de recessus tussen het antero-inferieure gedeelte van de Achillespees

en de posterosuperieure gedeelte van de calcaneus (retrocalcaneaire recessus). Superficiele

calcaneaire bursitis: inflammatie van de bursa tussen een calcaneaire prominentie of de

Achillespees en de huid. Er wordt voorgesteld om eerdere termen als Haglund’s ziekte,

222

Haglund’s syndroom, Haglund’s deformiteit, calcaneus altus, komkommerhiel en knobbelhiel

niet meer te gebruiken.

hoofDstUk 2

Uitkomstmaten en onderzoeksinstrumentenEen uitgebreide anamnese en lichamelijk onderzoek zijn essentieel in de diagnose van Achil-

les tendinopathie. Verder is het belangrijk om continu de voortgang van de patiënt te docu-

menteren met gevalideerde functionele tests en uitkomstmaten zoals de VISA-A vragenlijst.

Ook algemene klachten van pijn en functie en de mogelijkheid terug te keren naar eerdere

activiteiten en sport zijn belangrijke maten. Dit geldt niet alleen voor wetenschappelijke

doeleinden, maar ook voor de behandelend therapeut of arts om de voortgang van de

behandeling en revalidatie te kunnen volgen.

hoofDstUk 3

Vertaling en validatie van de Nederlandse VISA-A vragenlijst en zijn toepasbaarheid bij niet-sportersDe VISA-A (Victorian Institute of Sports Assessment- Achilles) vragenlijst is ontworpen in

2001 om de klinische ernst van Achilles tendinopathie te meten. Het is een vragenlijst welke

symptomen en het effect ervan op lichamelijke activiteit evalueert en wordt door patiënten

zelf ingevuld. In dit hoofdstuk hebben we getracht de vragenlijst in het Nederlands te vertalen

en te valideren om hem ook bruikbaar te maken voor onze patiëntenpopulatie. Na vertaling

volgens een voorwaarts- achterwaarts protocol, werden 101 patiënten met klachten van

Achilles tendinopathie geïncludeerd. Zij vulden de VISA-A-NL vragenlijst in op 2 verschil-

lende momenten, tegelijk met VAS, FAOS en SF-36 vragenlijsten. Betrouwbaarheid, interne

consistentie en de validiteit van construct- en inhoud werden getest. De VISA-A-NL bewijst

een uitstekend instrument to zijn voor het evalueren van klachten voor de Nederlandse arts.

Wanneer deze gebruikt gaat worden bij niet-sporters wordt aanbeloven een gemodificeerde

score (vragen 1-6) te gebruiken. Correlatie van VISA-A-NL met andere vragenlijsten was

gematigd of minder.

hoofDstUk 4

Minder gunstige resultaten met scleroserende Etoxysclerol injecties bij patiënten met Achilles tendinopathie: een retrospectief onderzoekBij patiënten met chronische klachten van Achilles tendinopathie wordt neovascularisatie

in de omgeving van de Achillespees gezien, maar niet bij pijnvrije normale pezen. Lokale

injectie van de scleroserende substantie Etoxysclerol hebben goede resultaten laten zien. Na

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een intensieve training door de bedenkers van de behandeling, werden in ons centrum 48

patiënten (53 pezen) behandeld met Etoxysclerol. Zes weken na de laatste injectie had maar

44% minder of geen klachten meer. Na een follow-up van 2.7-5.1 jaar, heeft 53% aanvul-

lende behandelingen gehad, en 3 van deze patiënten (7.5%) heeft nog steeds klachten.

Gezien deze uitkomst hebben wij de eerder behaalde voordelige resultaten niet kunnen

bevestigen.

hoofDstUk 5

Tendoscopie aan enkel en voetIn tegenstelling tot de arthroscopie, welke de techniek van voorkeur is geworden voor de

behandeling van intra-articulaire enkelproblematiek, worden extra- articulaire problemen van

de enkel traditioneel benaderd middels open chirurgie. Open chirurgie van de enkel is eerder

geassocieerd met complicaties zoals schade aan de nervus suralis en – peroneus superficialis,

infectie, littekenvorming en stijfheid van het enkelgewricht. Het percentage gerapporteerde

complicaties voor bijvoorbeeld posterieure enkel impingement varieert tussen de 15 en 24%.

De incidentie van deze complicaties heeft de ontwikkeling van extra-articulaire scopische

technieken gestimuleerd. Deze technieken hebben voordelen die gerelateerd zijn aan de

meeste minimaal invasieve procedures zoals minder wondinfecten en bloedverlies, kleiner

wondoppervlak en lagere morbiditeit. Nabehandeling is functioneel, en de ingrepen kunnen

in dagbehandeling gedaan worden.

Endoscopie van de pees, tendoscopie, wordt gedaan om verschillende pathologische aan-

doeningen te diagnosticeren en te behandelen. Indicaties voor, en de techniek van Achilles-,

peroneus, - en tibialis posterior tendosocopie, worden beschreven in dit hoofdstuk. Allen

laten op de korte- en langere termijn goede resultaten zien.

hoofDstUk 6

De relatie tussen Achilles- en plantarispees: een anatomische studie De pijnklachten bij midgedeelte Achilles tendinopathie is meest prominent aan de mediale

zijde van de Achillespees, waar ook in de meeste gevallen degeneratieve afwijkingen gezien

worden. Tijdens Achilles tendoscopie zien we dat de plantarispees gefixeerd is aan de Achil-

lespees ter hoogte van de klachten. Bij chronische inflammatie zouden adhesies tussen Achil-

les- en plantarispees, welke collectief in één peritendineum lopen, gevormd kunnen worden.

De Achillespees is betrokken bij plantairflexie, waar de plantarispees ook een klein deel

van de inversie van de enkel verzorgt. Als er adhesies bestaan, kunnen deze tegengestelde

krachten in theorie klachten veroorzaken. Het doel van deze studie was om de anatomische

positie van de plantarispees en de relatie ervan met de Achillespees te bepalen. In tegenstel-

ling tot wat de literatuur beschrijft, werd bij alle preparaten een plantarispees gevonden.

224

Negen verschillende inserties zijn gezien; meestal mediaal en waaiervormig op de calcaneus.

Bij 11 preparaten werden verbindingen gevonden tussen Achilles- en plantarispees, welke

zouden kunnen bijdragen aan het ontstaan van klachten.

hoofDstUk 7

Goede uitkomst na het strippen van de plantarispees als behandeling van patiënten met midgedeelte Achilles tendinopathieMidgedeelte Achilles tendinopathie is doorgaans moeilijk te behandelen. De pijn is meestal

gelokaliseerd aan de mediale zijde van de pees. Hier loopt ook de plantarispees. Onze hypoth-

ese was dat geisoleerd strippen van de plantarispees voldoende is om klachten te behan-

delen. Bij 3 patiënten werd de plantarispees geëxcideerd. Pre-operatief hadden zij klachten

van pijn bij palpatie van de mediale zijde van de Achillespees met nodulaire verdikking ter

plaatse. MRI liet betrokkenheid van de plantarispees in het proces zien. De plantarispees

werd stomp opgezocht en geëxcideerd met een peesstripper door een incisie van 3 cm in

het proximale gedeelte van de kuit. De 3 patiënten in deze publicatie hadden een goede of

uitstekende uitkomst. Mediale pijn zou dus gebaseerd kunnen zijn op betrokkenheid van de

plantarispees in het proces, maar goed uitgevoerde studies zullen moeten plaatshebben om

deze hypothese te bevestigen.

hoofDstUk 8

Midgedeelte Achilles tendinopathie: waarom pijnlijk? Een evidence-based filosofieVerscheidene factoren spelen een rol in de oorzaak van de pijn van patiënten met midgedeelte

Achilles tendinopathie. Als de behoeften van de pees groter zijn dan deze aankan, ontstaat

er microschade. Het lichaam reageert met een reparatieproces welke faalt bij patiënten met

tendinopathie. Dit veroorzaakt inadequate collageen en matrixproductie, tenocyt disruptie,

een verdere vermindering van functioneel collageen en matrix en een verhoogde kwets-

baarheid voor meer microschade. Het paratenon veroorzaakt ingroei van vaten om het

defect te repareren. Deze bloedvaten worden vergezeld door sensibele neo-zenuwen, welke

een verhoging in pijnsignalering door de productie van nociceptieve substanties voorbij de

kritieke drempel induceert. Myofibroblasten prolifereren welke overvloedige hoeveelheden

collageen synthetiseren om het peeslichaam te repareren; maar ook zorgen ook voor het

ontstaan van littekenweefsel waardoor het paratenon aan de Achillespees vast komt te

zitten. Fibrosering veroorzaakt dan weer constrictie van vasculaire kanalen en daarmee

beknelling van de toevoer van nutriënten waardoor bloedvaten oblitereren. Zenuwen zullen

achterblijven.

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Pijn is meestal aanwezig aan de mediale zijde van de pees. Dit is waar de plantarispees

ook loopt. Adhesies tussen de beide pezen obstrueren de tegengestelde krachten van deze

bi- en triarticulaire spiergroepen. Herhaalde trekkracht aan dit rijk-geïnnerveerde gebied kan

toevoegen aan de mediaal gelokaliseerde pijn en stijfheid tijdens en na het bewegen.

hoofDstUk 9

De belaste laterale röntgenfoto bij een retrocalcaneaire bursitisEen chronische retrocalcaneaire bursitis wordt veroorzaakt door herhaaldelijke beklem-

ming van de retrocalcaneaire bursa tussen Achillespees en posterosuperieure calcaneus. Bij

lichamelijk onderzoek is er lateraal en mediaal van de Achillespees een prominente zwelling

palpabel juist proximaal van de calcaneus. Standaard laterale en anteroposterieure röntgen-

opnamen van de enkel worden doorgaans gemaakt om voetdeformiteiten en benige afwi-

jkingen uit te sluiten. Om de diagnose van een retrocalcaneaire bursitis te bevestigen, wordt

een echo, MRI of zelfs een botscan gemaakt. Dit hoofdstuk beschrijft de hoge bruikbaarheid

van een weke delen- zwelling in de retrocalcaneaire recessus op een standaard belaste

laterale röntgenfoto van de enkel bij patiënten met een retrocalcaneaire bursitis. Kostbaar

en tijdsintensief aanvullend onderzoek is door gebruik van dit diagnostisch hulpmiddel niet

meer nodig.

hoofDstUk 10

Endoscopische calcaneoplastiekAls maximale conservatieve behandeling voor een retrocalcaneaire bursitis faalt, kan chirur-

gisch ingrijpen overwogen worden. Meestal worden open ingrepen gedaan; in onze kliniek is

in 2001 de endoscopische calcaneoplastiek geïntroduceerd. Er worden 2 portals gebruikt net

lateraal en mediaal van de Achillespees, juist proximaal van het posterosuperieure gedeelte

van de calcaneus. Tijdens de procedure worden de retrocalcaneaire bursa, posterosuperieure

tuberositas van de calcaneus en synovitis gereseceerd. De resultaten zijn goed, nabehandel-

ing is functioneel en patiënten kunnen snel hun normale activiteiten hervatten.

hoofDstUk 11

Optimalisatie van portalplaatsing bij endoscopische calcaneoplastiekDoor de lokale anatomie en zwelling is het palperen van het posterosuperieure gedeelte van

de calcaneus bemoeilijkt en kunnen de 2 portals te proximaal geplaatst worden. De calcaneus

kan hierdoor niet behoorlijk bereikt worden, wat resulteert in een suboptimale procedure of,

als het probleem herkend wordt, de noodzaak om de incisies opnieuw te maken of te ver-

lengen. Standaardiseren van de locatie van de portals lijkt essentieel. In dit hoofdstuk hebben

226

we daarom de afstand van de fibulatip tot de posterosuperieure calcaneus bij verschillende

voetvormen gemeten, om als hulpmiddel bij portalplaatsing te dienen. Locatie van portals bij

patiënten met platvoeten zou op gemiddeld 15 mm van de fibulatip moeten zijn, bij normale

voeten op 20 mm, en bij cavus voeten op een gemiddelde van 22 mm, alles distaal van de

tip. De verschillende voetvormen lieten een duidelijke overlap zien tussen de afstanden van

fibulatip tot calcaneus, maar we kunnen concluderen dat in vergelijk met cavus voeten, bij

platvoeten de portals significant meer proximaal van de fibulatip gemaakt moeten worden.

ALGemeNe DiscUssie

Voor de behandeling van de verschillende typen Achilles tendinopathie geoptimaliseerd kan

worden, moeten sommige basale zaken in acht genomen worden. Ten eerste is het van

waarde allemaal dezelfde taal te gaan spreken, wat belangrijk is in de wetenschap maar

ook in de dagelijkse praktijk. Wereldwijde standaard terminologie en gevalideerde uitkomst-

maten voor sporters en niet-sporters zijn de eerste stappen. Voorts moet de oorzaak van de

klachten gevonden worden. Hoewel dit bij elke pathologie de meest belangwekkende zaak

is, zou het ons zo helpen de juiste en zelfs geïndividualiseerde behandelstrategieën te vinden.

Sclerosering van neovascularisatie leek veelbelovend maar is niet de oplossing gebleken.

Een poging is gewaagd het focus van intratendineuze afwijkingen te verleggen naar het

paratenon en de plantarispees door het formuleren van een evidence-based filosofie. Meer

onderzoek is nodig om deze hypothese the bevestigen.

Bij een retrocalcaneaire bursitis is het maken van een MRI niet meer zinvol gebleken; met

adequate anamnese en lichamelijk onderzoek en een digitale röntgenfoto van de voet kan

de diagnose goed gesteld worden. De waarde van deze röntgenfoto na eerdere chirurgische

ingrepen aan de achtervoet wordt momenteel uitgezocht. De endoscopische calcaneoplas-

tiek moet gestandaardiseerd worden omdat zwelling en lokale anatomie portalplaatsing

bemoeilijken. Bij patiënten met platvoeten moeten portals meer proximaal geplaatst worden

dan bij cavus voeten; hoewel de onderzoekspopulatie vergroot moet worden om een sig-

nificant verschil te vinden tussen alle voetmorfologieën. Tot die tijd wordt aanbevolen dat

minder ervaren chirurgen hun portals maken onder beeldversterking.

Addendum

Bibliography

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PUBLicAtioNs AND PreseNtAtioNs reLAteD to this thesis

MN van Sterkenburg, CN van Dijk. Mid- Portion Achilles Tendinopathy: Why Painful? An

evidence based philosophy. Knee Surg Sports Traumatol Arthrosc 2011;19(8):1367-1375

MN van Sterkenburg, GMMJ Kerkhoffs, CN van Dijk. Good outcome after stripping the

plantaris tendon in patients with chronic mid-portion Achilles tendinopathy. Knee Surg

Sports Traumatol Arthrosc 2011;19(8):362-1366

MN van Sterkenburg, M Groot, IN Sierevelt, GMMJ Kerkhoffs, CN van Dijk. Optimization

of Portal Placement for Endoscopic Calcaneoplasty. Arthroscopy 2011;27(8):1110-1117

MN van Sterkenburg, IN Sierevelt, JL Tol, IV van Dalen, D Haverkamp, CN van Dijk.

Translation and validation of the Dutch version of the VISA-A questionnaire and applicability

to non-athletes. Submitted

CN van Dijk, MN van Sterkenburg, JI Wiegerinck, J Karlsson, N Maffulli. Terminology for

Achilles tendon related disorders. Knee Surg Sports Traumatol Arthrosc 2011;19(5):835-41

MN van Sterkenburg, CN van Dijk. Injection treatment for chronic midportion Achilles

tendinopathy: do we need that many alternatives? Knee Surg Sports Traumatol Arthrosc.

2011 Apr;19(4):513-5

MN van Sterkenburg, GMMJ Kerkhoffs, RP Kleipool, CN van Dijk. The plantaris tendon and

a potential role in mid-portion Achilles tendinopathy: an observational anatomical study. J

Anat. 2011; 218(3):336-41

MN van Sterkenburg, MC de Jonge, IN Sierevelt, CN van Dijk. Less Promising Results with

Sclerosing Etoxysclerol Injections for Mid-portion Achilles Tendinopathy: a Retrospective

Study. Am J Sports Med 2010; 38 (11): 2226-32

MN van Sterkenburg, B Muller, M Maas, IN Sierevelt, CN van Dijk. Appearance of the

weight-bearing lateral radiograph in retrocalcaneal bursitis. Acta Orthopaedica 2010; 81:

387–390

MN van Sterkenburg, PAJ de Leeuw, CN van Dijk. Tendoskopie am Sprunggelenk und Fuß.

Arthroskopie 2009;22:132-140

K Gravare Silbernagel, MN van Sterkenburg, J Karlsson. Diagnosis. Achilles Tendinopathy:

Current Concepts 2010:35-40

MN van Sterkenburg, M Paavola, CN van Dijk. Paratendinopathy. Achilles Tendinopathy:


MN van Sterkenburg, H Thermann, CN van Dijk. Achilles Tendoscopy. Achilles Tendinopa-

thy: Current Concepts 2010:151-155

MN van Sterkenburg, J Karlsson, CN van Dijk. Sport Specific Issues. Achilles Tendinopathy:


K Gravare Silbernagel, MN van Sterkenburg, A Brorsson, J Karlsson. Outcome Measures

and Assessment Tools. Achilles Tendinopathy: Current Concepts. 2010:205-212

232

MN van Sterkenburg, PAJ de Leeuw, CN van Dijk. Endoscopic Calcaneoplasty. In press

Minimally Invasive Surgery of the Foot and Ankle, editors Maffulli & Easley

MN van Sterkenburg. Achilles tendinopathy: peritendinous changes [invited lecture].

Scientific Meeting Vereniging voor Sportgeneeskunde 2011, Bilthoven

MN van Sterkenburg, M Groot, IN Sierevelt, GMMJ Kerkhoffs, CN van Dijk. Optimization

of portal placement for endoscopic calcaneoplasty. Biannual ESSKA meeting 2010, Oslo,

Norway

MN van Sterkenburg, B Muller, M Maas, IN Sierevelt, CN van Dijk. The Aspect of the

Retrocalcaneal Recess of Kager’s triangle: a Reliable Diagnostic Criterion for Retrocalcaneal

Bursitis. Biannual ESSKA meeting 2010, Oslo, Norway

MN van Sterkenburg, B Muller, M Maas, IN Sierevelt, CN van Dijk. Kager’s Triangle: a Useful

Diagnostic Criterion for Retrocalcaneal Bursitis. Minimally Invasive Surgery of Foot and Ankle

(MISFA) meeting 2009, Murcia, Spain

MN van Sterkenburg, B Muller, M Maas, IN Sierevelt, CN van Dijk. Kager’s Triangle: a Useful

Diagnostic Criterion for Retrocalcaneal Bursitis. Jaarvergadering Nederlandse

Orthopaedische Vereniging (NOV) 2009, Den Bosch

MN van Sterkenburg, GMMJ Kerkhoffs, RJ Oostra, CN van Dijk. Involvement of the Plan-

taris Tendon in Achilles Tendinopathy: an Anatomical Observational Study. Biannual ESSKA

meeting 2010, Oslo, Norway

MN van Sterkenburg, GMMJ Kerkhoffs, CN van Dijk. Achilles Tendinopathy: Stripping the

Plantaris Tendon Results in a Good to Excellent Outcome. A Report of 3 Cases. Biannual

ESSKA meeting 2010, Oslo, Norway

MN van Sterkenburg, MC de Jonge, IN Sierevelt, CN van Dijk. Sclerosing Polidocanol Injec-

tions in Achilles Tendinopathy: A Retrospective Study. Nordic Orthopaedic Federation (NOF)

meeting 2008, Amsterdam

Additional publications MN van Sterkenburg, CJA van Bergen, GMMJ Kerkhoffs. Juvenile Wakeboarder Locks Ankle

on Shore. Knee Surgery Sports Traumatology and Arthroscopy 2010 Dec;18(12):1661-3.

ML Reilingh, MN van Sterkenburg, PAJ de Leeuw, CN van Dijk. Tendoscopy of Posterior

Tibial and Peroneal Tendons. Techn Foot Ankle Surg 2010; 9:43-47

MN van Sterkenburg, D Haverkamp, CN van Dijk, GMMJ Kerkhoffs. A Posterior Tibial

Tendon Skipping Rope. Knee Surg Sports Traumatol Arthrosc 2010; 18(12): 1664-66

PAJ de Leeuw, MN van Sterkenburg, CN van Dijk. Arthroscopy and endoscopy of the Ankle

and Hindfoot. Sports Medicine and Arthroscopy 2009;17:175-184

H Davies, BR Tietjens, MN van Sterkenburg, A Mehgan. Anterior Cruciate Ligament Injuries

in Snowboarders: a Quadriceps induced Injury. Knee Surgery Sports Traumatol Arthrosc

2009;17:1048-51

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ML Reilingh, MN van Sterkenburg, PAJ de Leeuw, IV van Dalen, CN van Dijk. Ankle

Arthroscopy, Indications, Technique and Complications. South African Orthopaedic Journal

2009;8:51-58

GJM Tuijthof, MN van Sterkenburg, IN Sierevelt, GMMJ Kerkhoffs, CN van Dijk. First

Experience with a Physical Simulation Environment for Training of Arthroscopic Skills. Knee

Surg Sports Traumatol Arthrosc 2010;18:218-224

CJA van Bergen, M Zengerink, L Blankevoort, MN van Sterkenburg, J van Oldenrijk, CN van

Dijk. Novel Metallic Implantation Technique for Osteochondral Defects of the Medial Talar

Dome: A Biomechanical Cadaveric Study. Acta Orthop. 2010 Aug;81(4):495-502

CN van Dijk, PAJ de Leeuw, MN van Sterkenburg. Tendoscopy AANA Advanced Arthros-

copy: the Foot and Ankle, editors Amendola, Ryu, Stone

ML Reilingh, PAJ de Leeuw, MN van Sterkenburg, CN van Dijk. Posterior Ankle Arthroscopy

and Tendoscopy. Sports Medicine Volume in the Master Techniques series, editor Fu, 2011

PAJ de Leeuw, MN van Sterkenburg, CJA van Bergen, CN van Dijk. Posterior Ankle Arthros-

copy and Endoscopy. In press International Advances in Foot & Ankle Surgery, editor Saxena

MN van Sterkenburg, PAJ de Leeuw, CN van Dijk. Tendoscopy. In press Minimally Invasive

Surgery of the Foot and Ankle, editors Maffulli & Easley

J Karlsson, MN van Sterkenburg, GMMJ Kerkhoffs, CN van Dijk. Open Surgery for Achil-

les Tendon Rupture. Achilles Tendon Rupture: Current Concepts 2008;1st edition:50-56, 2nd

edition:49-56

MN van Sterkenburg, B Donley, CN van Dijk. Guidelines for Sport Resumption Follow-

ing Achilles Tendon Rupture. Achilles Tendon Rupture: Current Concepts 2008;1st edi-

tion:108-117, 2nd edition:107-116

MN van Sterkenburg, CN van Dijk. Overview of Reviews on the Treatment of Acute Achilles

Tendon Ruptures. Achilles Tendon Rupture: Current Concepts 2008;1st edition:34-48, 2nd

edition:33-47

Dankwoord

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Prof. dr. C.N. van Dijk, promotor en opleider. Allereerst wil ik u bedanken. De bijna drie

jaar die ik fulltime onderzoek heb gedaan, waren jaren waarin u mij barstensvol energie en

oceanen aan nieuwe ideeën hielp. De vele besprekingen die meestal tegen de deurpost van

mijn ‘kamer’ plaatsvonden, waren aanleiding voor nieuwe inspiratie. Maar ook lastminute

congresbezoeken zorgden er op wonderlijke wijze voor dat de wetenschappelijke moed,

die soms ver in mijn schoenen gezakt was, een extra stimulus kreeg. Alles heeft geresult-

eerd in dit proefschrift en een royaal archief aan digitaal beeldmateriaal. Van uw talent om

gedrevenheid tot het maximum te sturen, hoop ik nog veel gebruik te mogen maken. Ik zie

uit naar de voortzetting van onze samenwerking dit jaar.

Dr. G.M.M.J. Kerkhoffs, co-promotor, Gino. Elke alinea kritisch tegen het licht gehouden,

alle vergeten letters opgespoord, elke referentie bekeken. Toen jij terug kwam naar het

AMC was mijn onderzoek al geruime tijd van start, maar door jouw visie heeft het een

vogelvlucht genomen. Je kunt bij herhaling dezelfde vraag stellen zodat een korte veronder-

stelling verandert in een groot wetenschappelijk project, ofwel in een gedachtewisseling

over persoonlijker levensvragen. Als orthopedisch chirurg maar ook in sociale zin ben je een

inspirator. Dank je wel voor de afgelopen jaren, zin in de komende.

Leden van de promotiecommissie, bestaande uit prof. dr. F.J.G. Backx, prof. dr. R.L.

Diercks, prof. dr. J.C. Goslings, dr. M. Maas, prof. dr. R.J. Oostra en prof. dr. R.J.P.M.

Scholten. U wil ik bedanken voor het beoordelen van het manuscript en ik zie uit naar de

aanstaande academische discussie.

Dr. ir. L. Blankevoort, Leendert. Dank voor je financiële begeleiding en minutieuze weten-

schappelijke kritiek tijdens de algemene onderzoeksbesprekingen.

Drs. I.N. Sierevelt, Inger. Allereerst veel dank voor je hulp bij de methodologie en statistiek

van mijn studies. Je bent van bijzondere waarde voor de ORCA. Daarnaast heb ik goede

herinneringen aan onze vele kilometers hardlopen tijdens lunchpauzes. Je had gewoon mee

moeten gaan naar New York.

Dr. I.V. van Dalen, dr. D. Haverkamp, drs. M.C. de Jonge, drs. R.P. Kleipool, dr. M.

Maas, dr. J.L. Tol. Dank voor jullie waardevolle bijdrage aan dit proefschrift.

Marga en Rosalie. Veel dank voor alle ondersteuning bij administratieve zaken.

Rogier van Sterkenburg en Jan Joost Wiegerinck. Mijn paranimfen. Hoe moet ik jullie

nou in één alinea bedanken? Rogier, vroeger al erg druk met je zusje; van voorlezen via tech-

nisch lego tot wiskundeboek. Van mijn drie broers viel de keuze op jou, omdat ik verwachtte

238

dat jij het meest enthousiast aan de slag zou gaan met je taak als mijn paranimf. En die

gedachte bleek al juist op de dag dat ik je vroeg. Jan Joost, mijn opvolger in de Achillespees-

lijn. Indrukwekkend hoe jij het binnen een aantal maanden presteerde van een bescheiden

opzet genoeg plannen te maken voor 3 proefschriften. Ik denk dat wij naast collega’s goede

vrienden zijn geworden. Bovenal heb je aardig leren photoshoppen.

G4/ De kweekvijver: Jakob, Christiaan, Peter, Job, Sjoerd, Mikel, Bas, Laurens en

Gabriëlle. Wat een mooie avonturen hebben wij beleefd. Een onverstaanbaar congres in

Murcia, AAOS in New Orleans, met Job de marathon van New York, met Chris en Jakob in

de vooropleiding. Er zullen er nog heel veel volgen.

Collega’s Heelkunde Beverwijk. Huib, bedankt voor je positieve wetenschappelijke

beoordelingen ondanks dat er in het RKZ geen enkel onderzoek uit mijn handen kwam.

Is je boekje al af? Dit is hem dan. Wat een ontzettend leuke werksfeer en ik zal de laatste

maanden nog uitgebreid genieten. Vrij van proefschrift.

Vrienden. Bedankt dat jullie er zijn; voor jullie afleiding, interesse, vele glazen bier en wijn

en geweldige kookkunsten.

Broers, schoonzussen, neefjes en nichtjes. Ja heren, als jullie het niet doen, doet jullie

zusje het wel. Of begint het toch te kriebelen? Op nog heel veel mooie momenten samen.

Misschien is het nu tijd jullie te evenaren in de volgende levensfase.

Papa en mama. Vijf jaar geleden hadden jullie deze niet aan zien komen. Vijftién jaar

geleden allerminst. En toch is het gelukt. In de wetenschappelijke voetsporen van vader.

Geniet ervan. Ik hou van jullie.

Part VI

Cu

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cUrricULUm vitAe

Maayke Nadine van Sterkenburg was born on July 11th, 1981 in Leiderdorp, the Netherlands.

After graduating from high school (Gymnasium, Rijnlands Lyceum Oegstgeest), she started

Medical School at the University of Amsterdam. A 5-month internship in Orthopedic Surgery

in Auckland, New Zealand (Prof. Dr. B.R. Tietjens) made her enthousiastic to continue in this

working field. She worked three years as a research fellow at the Department of Orthopedic

Surgery of the Academical Medical Center in Amsterdam (Head: Prof. Dr. C.N. van Dijk)

which resulted in this thesis. In July she will finish a 2-year residency in General Surgery at

the Rode Kruis Ziekenhuis Beverwijk (Head: Dr. H.A. Cense) and return to the Academical

Medical Center Amsterdam for her training in Orthopedic Surgery under supervision of Prof.

Dr. C.N. van Dijk.

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